Ebook Contemporary oral and maxillofacial surgery: Part 2

Part

IV
Infections

Odontogenic infections are generally caused by bacteria that
have a propensity to cause abscess formation. In addition, the
roots of the teeth provide a pathway for infecting bacteria to
enter the deep tissues of the periodontium and periapical
regions. Therefore, odontogenic infections cause deep-seated
abscesses, and they almost always require some form of surgical therapy. Treatments range from endodontic therapy and
gingival curettage to extraction, incision, and drainage of the
deep fascial spaces of the head and neck. Antibiotic therapy
is an adjunctive treatment to the required surgery. Prophylactic antibiotic therapy may prevent distant infections caused by
bacteremias arising from oral-maxillofacial surgical procedures, and such therapy may also prevent some postoperative
wound infections.
This section presents the principles of management and
prevention of infections in dental patients.
Chapter 16 describes the basic management techniques,
including surgery and antibiotic administration, in the treatment of odontogenic infections. This chapter also discusses
the principles of antibiotic prophylaxis for the prevention of
wound infection and distant metastatic infection such as
infectious endocarditis.
Chapter 17 presents an overview of complex odontogenic
infections that involve the deep fascial spaces, which may
necessitate hospitalization of the patient. Osteomyelitis and
other unusual infections are also discussed.

Chapter 18 presents the indications, rationale, and technical aspects of surgical endodontics. Although periapical
surgery is occasionally necessary for successful endodontic
management, it is necessary for the clinician to choose this

treatment modality wisely. Therefore, the discussion of the
indications and contraindications for endodontic surgery is
extensive, and the technical aspects of surgical endodontics
are well illustrated.
Chapter 19 presents information about patients at risk for
infection and other problems that are caused by compromise
of the patient’s host defense as a result of radiotherapy or
cancer chemotherapy. These patients are susceptible to a
variety of problems, and the prevention and management of
these problems are discussed.
Chapter 20 describes maxillary sinus problems that arise
from odontogenic infections and other problems. Although
general practitioners rarely see patients with these problems,
they may have to provide diagnoses before referring these
patients to the appropriate health care professional for
definitive care.
Finally, Chapter 21 discusses salivary gland diseases, primarily the obstructive and infectious types. The major diagnostic and therapeutic modalities used in managing these
problems are discussed.

295


Chapter

16 

Principles of Management and Prevention of
Odontogenic Infections
Thomas R. Flynn

CHAPTER OUTLINE
MICROBIOLOGY OF ODONTOGENIC INFECTIONS  297
NATURAL HISTORY OF PROGRESSION OF ODONTOGENIC
INFECTIONS  298
PRINCIPLES OF THERAPY OF ODONTOGENIC
INFECTIONS  299
Principle 1: Determine Severity of Infection  300
Complete History  300
Physical Examination  300

Principle 2: Evaluate State of Patient’s Host Defense
Mechanisms  302
Medical Conditions That Compromise Host Defenses  302

Principle 2: Choose Correct Antibiotic  313
Principle 3: Antibiotic Plasma Level Must Be High  313
Principle 4: Time Antibiotic Administration Correctly  313
Principle 5: Use Shortest Antibiotic Exposure That Is
Effective  313
Summary  313
PRINCIPLES OF PROPHYLAXIS AGAINST METASTATIC
INFECTION  314
Prophylaxis Against Infectious Endocarditis  314
Prophylaxis in Patients with Other Cardiovascular
Conditions  316
Prophylaxis Against Total Joint Replacement
Infection  316

Pharmaceuticals That Compromise Host Defenses  302

Principle 3: Determine Whether Patient Should Be
Treated by General Dentist or Oral-Maxillofacial
Surgeon  303
Principle 4: Treat Infection Surgically  304
Principle 5: Support Patient Medically  306
Principle 6: Choose and Prescribe Appropriate
Antibiotic(s)  306
Determine the Need for Antibiotic Administration  306
Use Empirical Therapy Routinely  307
Use the Narrowest-Spectrum Antibiotic  308
Use the Antibiotic with the Lowest Incidence of Toxicity and Side
Effects  308
Use a Bactericidal Antibiotic, if Possible  309
Be Aware of the Cost of Antibiotics  309
Summary  309

Principle 7: Administer Antibiotic Properly  310
Principle 8: Evaluate Patient Frequently  311
PRINCIPLES OF PREVENTION OF INFECTION  311
PRINCIPLES OF PROPHYLAXIS OF WOUND
INFECTION  312
Principle 1: Procedure Should Have Significant Risk of
Infection  312
296

In dentistry, one of the most difficult problems to manage is an
odontogenic infection. Odontogenic infections arise from teeth and
have a characteristic flora. Caries, periodontal disease, and pulpitis
are the initiating infections, that can spread beyond teeth to the
alveolar process and to the deeper tissues of the face, oral cavity, head,

and neck. These infections may range from low-grade, well-localized
infections that require only minimal treatment to severe, lifethreatening deep fascial space infections. Although the overwhelming
majority of odontogenic infections are readily managed by minor
surgical procedures and supportive medical therapy that includes
antibiotic administration, the practitioner must constantly bear in
mind that these infections occasionally become severe and life
threatening within a short time.
This chapter is divided into several sections. The first section discusses the typical microbiologic organisms involved in odontogenic
infections. Appropriate therapy of odontogenic infections depends
on a clear understanding of the causative bacteria. The second section
discusses the natural history of odontogenic infections. When infections occur, they may erode through bone and into the adjacent soft
tissue. Knowledge of the usual pathway of infection from the teeth
and surrounding tissues through bone and into the overlying soft
tissue planes is essential when planning appropriate therapy. The
third section of this chapter deals with the principles of management
of odontogenic infections. A series of principles are discussed, with
consideration of the microbiology and typical pathways of infection.


Principles of Management and Prevention of Odontogenic Infections
The chapter concludes with a section on the prophylaxis of wound
infection and of metastatic infection.

MICROBIOLOGY OF ODONTOGENIC
INFECTIONS
The bacteria that cause infection are most commonly part of the
indigenous bacteria that normally live on or in the host. Odontogenic infections are no exception because the bacteria that cause
odontogenic infections are part of the normal oral flora: those that
comprise the bacteria of plaque, those found on mucosal surfaces,
and those found in the gingival sulcus. These bacteria are primarily

aerobic gram-positive cocci, anaerobic gram-positive cocci, and
anaerobic gram-negative rods. These bacteria cause a variety of
common diseases such as dental caries, gingivitis, and periodontitis.
When these bacteria gain access to deeper underlying tissues, as
through a necrotic dental pulp or through a deep periodontal pocket,
they cause odontogenic infections. As the infection progresses more
deeply, different members of the infecting flora can find better growth
conditions and begin to outnumber the previously dominant species.
Many carefully performed microbiologic studies of odontogenic
infections have demonstrated the microbiologic composition of
these infections. Several important factors must be noted. First,
almost all odontogenic infections are caused by multiple bacteria.
The polymicrobial nature of these infections makes it important that
the clinician understand the variety of bacteria that are likely to cause
infection. In most odontogenic infections, the laboratory can identify
an average of five species of bacteria. It is not unusual to identify as
many as eight different species in a given infection. On rare occasions, a single species may be isolated. New molecular methods,
which identify the infecting species by their genetic makeup, have
allowed scientists to identify greater numbers and a whole new range
of species, including unculturable pathogens, not previously associated with these infections. In the future, these methods may lead to
a completely new understanding of the pathogenesis of odontogenic
infections.
A second important factor is the oxygen tolerance of the bacteria
that cause odontogenic infections. Because the mouth flora is a combination of aerobic and anaerobic bacteria, it is not surprising to find
that most odontogenic infections are caused by anaerobic and aerobic
bacteria. Infections caused by aerobic bacteria alone account for 6%
of all odontogenic infections. Anaerobic bacteria alone are found in
44% of odontogenic infections. Infections caused by mixed anaerobic and aerobic bacteria comprise 50% of all odontogenic infections
(Table 16-1).
The predominant aerobic bacteria in odontogenic infections

(found in about 65% of cases) are the Streptococcus milleri group,
which consists of three members of the S. viridans group of bacteria:

Table 16-1  Role of Anaerobic Bacteria in
Odontogenic Infections
Percentage
Anaerobic only

50

Mixed anaerobic and aerobic

44

Aerobic only

6

Data from Brook I, Frazier EH, Gher ME: Aerobic and anaerobic microbiology
of periapical abscess. Oral Microbiol Immunol 6:123–125, 1991.

Chapter | 16 |

S. anginosus, S. intermedius, and S. constellatus. These facultative organisms, which can grow in the presence or the absence of oxygen, may
initiate the process of spreading into deeper tissue (Table 16-2).
Miscellaneous bacteria contribute 5% or less of the aerobic species
found in these infections. Rarely found bacteria include staphylococci, group D Streptococcus organisms, other streptococci, Neisseria
spp., Corynebacterium spp., and Haemophilus spp.
The anaerobic bacteria found in odontogenic infections include
an even greater variety of species (see Table 16-2). Two main groups,

however, predominate. The anaerobic gram-positive cocci are found
in about 65% of cases. These cocci are anaerobic Streptococcus and
Peptostreptococcus. Oral gram-negative anaerobic rods are cultured in
about three quarters of the infections. The Prevotella and Porphyro­
monas spp. are found in about 75% of these, and Fusobacterium
organisms are present in more than 50%.
Of the anaerobic bacteria, several gram-positive cocci (i.e., anaerobic Streptococcus and Peptostreptococcus spp.) and gram-negative rods
(i.e., Prevotella and Fusobacterium spp.) play a more important pathogenic role. The anaerobic gram-negative cocci and the anaerobic
gram-positive rods appear to have little or no role in the cause of
odontogenic infections; instead, they appear to be opportunistic
organisms.
The method by which mixed aerobic and anaerobic bacteria cause
infections is known with some certainty. After initial inoculation into
deeper tissues, the facultative S. milleri group organisms can synthesize hyaluronidase, which allows the infecting organisms to spread
through connective tissues, initiating the cellulitis stage of infection.
Metabolic byproducts from the streptococci create a favorable environment for the growth of anaerobes: the release of essential nutrients, lowered pH in the tissues, and consumption of local oxygen
supplies. The anaerobic bacteria are then able to grow, and as the
local oxidation–reduction potential is lowered further, the anaerobic
bacteria predominate and cause liquefaction necrosis of tissues by

Table 16-2  Major Pathogens in Odontogenic Infections
PERCENT OF CASES
Microorganism

Sakamoto
et al.* (1998)

Heimdahl
et al.† (1985)

Streptococcus
milleri group

65

31

Peptostreptococcus
species

65

31

Other anaerobic
streptococci

9

38

Prevotella species
(e.g., P. oralis
and P. buccae)

74

35

Porphyromonas

species (e.g.,
P. gingivalis)

17

–

Fusobacterium
species

52

45

*Data from Sakamoto H, Kato H, Sato T, Sasaki J: Semiquantitative
bacteriology of closed odontogenic abscesses. Bull Tokyo Dent Coll
39:103–107, 1998.
†
Heimdahl A, Von Konow L, Satoh T, et al: Clinical appearance of orofacial
infections of odontogenic origin in relation to microbiological findings. J Clin
Microbiol 22:299, 1985.

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Infections

their synthesis of collagenases. As collagen is broken down and

invading white blood cells necrose and lyse, microabscesses form and
may coalesce into a clinically recognizable abscess. In the abscess
stage, anaerobic bacteria predominate and may eventually become
the only organisms found in culture. Early infections appearing initially as a cellulitis may be characterized as predominantly aerobic
streptococcal infections, and late, chronic abscesses may be characterized as anaerobic infections.
Clinically, this progression of the infecting flora from aerobic to
anaerobic seems to correlate with the type of swelling that can be
found in the infected region. Thus, odontogenic infections seem to
pass through four stages. In the first 3 days of symptoms, a soft,
mildly tender, doughy swelling represents the inoculation stage, in
which the invading streptococci are just beginning to colonize the
host. After 3 to 5 days, the swelling becomes hard, red, and acutely
tender as the infecting mixed flora stimulates the intense inflammatory response of the cellulitis stage. At 5 to 7 days after the onset of
swelling, the anaerobes begin to predominate, causing a liquefied
abscess in the center of the swollen area. This is the abscess stage.
Finally, when the abscess drains spontaneously through skin or
mucosa, or it is surgically drained, the resolution stage begins as the
immune system destroys the infecting bacteria, and the processes of
healing and repair ensue. The clinical and microbiologic characteristics of edema, cellulitis, and abscess are summarized and compared
in Table 16-3.

Table 16-3  Comparison of Edema, Cellulitis, and Abscess

Characteristic

Edema
(Inoculation)

Cellulitis

Abscess

Duration

0–3 days

1–5 days

4–10 days

Pain, borders

Mild, diffuse

Diffuse

Localized

Size

Variable

Large

Smaller

Color

Normal

Red

Shiny center

Consistency

Jelly-like

Boardlike

Soft center

Progression

Increasing

Increasing

Decreasing

Pus

Absent

Absent

Present

Bacteria

Aerobic

Mixed

Anaerobic

Seriousness

Low

Greater

Less

A

NATURAL HISTORY OF PROGRESSION OF
ODONTOGENIC INFECTIONS
Odontogenic infections have two major origins: (1) periapical, as a
result of pulpal necrosis and subsequent bacterial invasion into the
periapical tissue, and (2) periodontal, as a result of a deep periodontal
pocket that allows inoculation of bacteria into the underlying soft
tissues. Of these two, the periapical origin is the most common in
odontogenic infections.
Necrosis of the dental pulp as a result of deep caries allows a
pathway for bacteria to enter the periapical tissues. Once this tissue
has become inoculated with bacteria and an active infection is established, the infection spreads equally in all directions, but preferentially along the lines of least resistance. The infection spreads through
the cancellous bone until it encounters a cortical plate. If this cortical
plate is thin, the infection erodes through the bone and enters the
surrounding soft tissues. Treatment of the necrotic pulp by standard

endodontic therapy or extraction of the tooth should resolve the
infection. Antibiotics alone may arrest, but do not cure, the infection
because the infection is likely to recur when antibiotic therapy has
ended without treatment of the underlying dental cause. Thus, the
primary treatment of pulpal infections is endodontic therapy or tooth
extraction, as opposed to antibiotics.
When the infection erodes through the cortical plate of the alveolar process, it spreads into predictable anatomic locations. The location of the infection arising from a specific tooth is determined by
the following two major factors: (1) the thickness of the bone overlying the apex of the tooth and (2) the relationship of the site of
perforation of bone to muscle attachments of the maxilla and
mandible.
Figure 16-1 demonstrates how infections perforate through bone
into the overlying soft tissue. In Figure 16-1, A, the labial bone overlying the apex of the tooth is thin compared with the bone on the
palatal aspect of the tooth. Therefore, as the infectious process
spreads, it goes into the labial soft tissues. In Figure 16-1, B, the tooth
is severely proclined, which results in thicker labial bone and a relatively thinner palatal bone. In this situation, as the infection spreads
through bone into the soft tissue, the infection is seen as a palatal
abscess.
Once the infection has eroded through bone, the precise location
of the soft tissue infection is determined by the position of the perforation relative to the muscle attachments. In Figure 16-2, A, the
infection has eroded through to the facial aspect of the alveolar
process and inferior to the attachment of the buccinator muscle,
which results in an infection that appears as a vestibular abscess. In

B

Figure 16-1  When infection erodes through bone, it will enter soft tissue through thinnest bone. A, Tooth apex is near thin labial bone, so infection
erodes labially. B, Right apex is near palatal aspect, so palatal bone will be perforated.

298

Principles of Management and Prevention of Odontogenic Infections

A

Chapter | 16 |

B

Figure 16-2  Relationship of point of bone perforation to muscle attachment determines fascial space involved. A, When tooth apex is lower than
muscle attachment, vestibular abscess results. B, If apex is higher than muscle attachment, the adjacent fascial space is involved.

Figure 16-3  Palatal abscess arising from the palatal root of a maxillary
first premolar.

Figure 16-2, B, the infection has eroded through the bone superior
to the attachment of the buccinator muscle and is expressed as an
infection of the buccal space because the buccinator muscle separates
the buccal and vestibular spaces.
Infections from most of the maxillary teeth erode through the
facial cortical plate. These infections also erode through the bone
below the attachment of the muscles that attach to the maxilla, which
means that most maxillary dental abscesses appear initially as vestibular abscesses. Occasionally, a palatal abscess arises from the apex
of a severely inclined lateral incisor or the palatal root of a maxillary
first molar or premolar (Fig. 16-3). More commonly, the maxillary
molars cause infections that erode through the bone superior to the
insertion of the buccinator muscle, which results in a buccal space
infection. Likewise, on occasion a long maxillary canine root allows
infection to erode through the bone superior to the insertion of the
levator anguli oris muscle and causes an infraorbital (canine) space

infection.
In the mandible, infections of incisors, canines, and premolars
usually erode through the facial cortical plate superior to the attachment of the muscles of the lower lip, resulting in vestibular abscesses.
Mandibular molar infections erode through the lingual cortical bone
more frequently than in the case of the anterior teeth. First molar
infections may drain buccally or lingually. Infections of the second
molar can perforate buccally or lingually (but usually lingually), and
third molar infections almost always erode through the lingual cortical plate. The mylohyoid muscle determines whether infections that

Figure 16-4  Vestibular abscess arising from maxillary incisor. Overlying
mucosa is thin because pus is near the surface. (From Flynn TR:
Anatomy of oral and maxillofacial infections. In Topazian RG, Goldberg
MH, Hupp JR, editors: Oral and maxillofacial infections, ed 4,
Philadelphia, PA, 2002, WB Saunders.)

drain lingually go superior to that muscle into the sublingual space
or below it into the submandibular space.
The most common odontogenic deep fascial space infection is a
vestibular space abscess (Fig. 16-4). Occasionally, patients do not
seek treatment for these infections, and the process ruptures spontaneously and drains, resulting in resolution or chronicity of the infection. The infection recurs if the site of spontaneous drainage closes.
Sometimes, the abscess establishes a chronic sinus tract that drains
to the oral cavity or to skin (Fig. 16-5). As long as the sinus tract
continues to drain, the patient experiences no pain. Antibiotic
administration usually stops the drainage of infected material temporarily, but when the antibiotic course is over, the drainage recurs.
Definitive treatment of a chronic sinus tract requires treatment of the
original causative problem, which is usually a necrotic pulp. In such
a case, the necessary treatment is endodontic surgery or extraction of
the infected tooth.

PRINCIPLES OF THERAPY OF ODONTOGENIC

INFECTIONS
This section discusses the management of odontogenic infections. A
series of principles are useful in treating patients who come to the
dentist with infections related to teeth and the gingiva. The clinician
must keep in mind the information in the preceding two sections of

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Infections

A
Figure 16-6  Patient with severe infection and elevated temperature,
pulse rate, and respiratory rate. The patient feels sick and tired; he has a
“toxic appearance.” (From Flynn TR: Surgical management of orofacial
infections. Atlas Oral Maxillofac Surg Clin North Am 8:79, 2000.)

B
Figure 16-5  Chronic drainage sinus tracts that result from low-grade
infections may drain intraorally (A) or extraorally (B). (A, Courtesy of
Sasha B. Ross, DMD. B, From Flynn TR, Topazian RG: Infections of the
oral cavity. In Waite D, editor: Textbook of practical oral and
maxillofacial surgery, Philadelphia, PA, 1987, Lea & Febiger.)

this chapter to understand these principles. By following these principles in a stepwise fashion, the clinician will certainly have met the
standard of care, even though the expected result may not always be
achieved. The first three principles are perhaps the most important
in determining the outcome, yet they can be accomplished by the

experienced practitioner within the first few minutes of the initial
patient encounter.

Principle 1: Determine Severity of Infection
Most odontogenic infections are mild and require only minor surgical therapy. When the patient comes for treatment, the initial goal is
to assess the severity of the infection. This determination is based on
a complete history of the current infectious illness and a physical
examination.
Complete history.  The history of the patient’s infection follows
the same general guidelines as those for any history. The initial
purpose is to find out the patient’s chief complaint. Typical chief
complaints of patients with infections are “I have a toothache,” “My
jaw is swollen,” or “I have a gum boil in my mouth.” The complaint
should be recorded in the patient’s own words.
The next step in history taking is determining how long the infection has been present. First, the dentist should inquire as to time of
onset of the infection. How long ago did the patient first have symptoms of pain, swelling, or drainage, which indicated the beginning
of the infection? The course of the infection is then discussed. Have
the symptoms of the infection been constant, have they waxed and
waned, or has the patient’s condition steadily grown worse since the

300

symptoms were first noted? Finally, the practitioner should determine
the rapidity of progress of the infection. Has the infection process
progressed rapidly over a few hours, or has it gradually increased in
severity over several days to a week?
The next step is eliciting information about the patient’s symptoms. Infections are actually a severe inflammatory response, and the
cardinal signs of inflammation are clinically easy to discern. These
signs and symptoms are, in Latin terms, dolor (pain), tumor (swelling),
calor (warmth), rubor (erythema, redness), and functio laesa (loss of

function).
The most common complaint is pain. The patient should be asked
where the pain actually started and how the pain has spread since it
was first noted. The second sign is tumor (swelling), which is a physical finding that is sometimes subtle and not obvious to the practitioner, although it is obvious to the patient. It is important that the
dentist ask the patient to describe any area of swelling. With regard
to the third characteristic of infection, calor (warmth), the patient
should be asked whether the area has felt warm to the touch. Redness
of the overlying area is the next characteristic to be evaluated. The
patient should be asked if there has been or is any change in color,
especially redness, over the area of the infection. Functio laesa (loss
of function) should then be checked. When inquiring about this
characteristic, the dentist should ask about trismus (difficulty opening
the mouth widely) and any difficulty chewing, swallowing (dysphagia), or breathing (dyspnea).
Finally, the dentist should ask how the patient feels in general.
Patients who feel fatigued, feverish, weak, and sick are said to have
malaise. Malaise usually indicates a generalized reaction to a moderateto-severe infection (Fig. 16-6).
In the next step, the dentist discusses treatment. The dentist
should find out about previous professional treatment and selftreatment. Many patients treat themselves with leftover antibiotics,
hot soaks, and a variety of other home or herbal remedies. Occasionally, a dentist may see a patient who had received treatment in an
emergency room 2 or 3 days earlier and was referred to a dentist by
the emergency room physician. The patient might have neglected to
follow the emergency room physician’s advice until the infection
became severe. Sometimes, the patient may not have taken the prescribed antibiotic because he or she could not afford to purchase it.
The patient’s complete medical history should be obtained in the
usual manner through an interview or a self-administered questionnaire with verbal follow-up of any relevant findings.
Physical examination.  The first step in the physical examination
is to obtain the patient’s vital signs, including temperature, blood
pressure, pulse rate, and respiratory rate. The need for evaluation of

Principles of Management and Prevention of Odontogenic Infections
temperature is obvious. Patients who have systemic involvement of
infection usually have elevated temperatures. Patients with severe
infections have temperatures elevated to 101°F or higher (greater
than 38.3°C).
The patient’s pulse rate increases as the patient’s temperature
increases. Pulse rates of up to 100 beats per minute (beats/min) are
not uncommon in patients with infections. If pulse rates increase to
greater than 100 beats/min, the patient may have a severe infection
and should be treated more aggressively.
The vital sign that varies the least with infection is the patient’s
blood pressure. Only if the patient has significant pain and anxiety
will an elevation occur in systolic blood pressure. However, septic
shock results in hypotension.
Finally, the patient’s respiratory rate should be closely observed.
One of the major considerations in odontogenic infections is the
potential for partial or complete upper airway obstruction as a result
of extension of the infection into the deep fascial spaces of the
neck. As respirations are monitored, the dentist should carefully
check to ensure that the upper airway is clear and that the patient
is able to breathe without difficulty. The normal respiratory rate is
14 to 16 breaths per minute (breaths/min). Patients with mild to
moderate infections may have elevated respiratory rates greater than
18 breaths/min.
Patients who have normal vital signs with only a mild temperature elevation usually have a mild infection that can be readily
treated. Patients who have abnormal vital signs with elevation of
temperature, pulse rate, and respiratory rate are more likely to have
serious infection and require more intensive therapy and evaluation
by an oral-maxillofacial surgeon.
Once vital signs have been taken, attention should be turned to

the physical examination of the patient. The initial portion of the
physical examination should be inspection of the patient’s general
appearance. Patients who have more than a minor, localized infection have an appearance of fatigue, feverishness, and malaise. This is
referred to as a “toxic appearance” (see Fig. 16-6).
The patient’s head and neck should be carefully examined for the
cardinal signs of infection (as discussed earlier), and the patient
should be inspected for any evidence of swelling and overlying erythema. The patient should be asked to open the mouth widely,
swallow, and take deep breaths so that the dentist can check for
trismus, dysphagia, or dyspnea. These are ominous signs of a severe
infection, and the patient should be referred immediately to an oralmaxillofacial surgeon or to the emergency room. A recent study of
severe odontogenic infections requiring hospitalization found
trismus (maximum interincisal opening less than 20 mm) in 73% of
cases, dysphagia in 78%, and dyspnea in 14%.
Areas of swelling must be examined by palpation. The dentist
should gently touch the area of swelling to check for tenderness,
amount of local warmth or heat, and the consistency of the swelling.
The consistency of the swelling may vary from very soft and almost
normal to a firmer, fleshy swelling (described as “doughy”) to an even
firmer or hard swelling (described as “indurated”). An indurated
swelling has similar firmness to a tightened muscle. Another characteristic consistency is fluctuance. Fluctuance feels like a fluid-filled
balloon. Fluctuant swelling almost always indicates an accumulation
of liquid pus in the center of an indurated area.
The dentist then performs an intraoral examination to try to find
the specific cause of the infection. Severely carious teeth, an obvious
periodontal abscess, severe periodontal disease, combinations of
caries and periodontal disease, or an infected fracture of a tooth or
the entire jaw may be present. The dentist should look and feel for
areas of gingival swelling and fluctuance and for localized vestibular
swellings or draining sinus tracts.
The next step is to perform a radiographic examination. This

usually consists of the indicated periapical radiographs. Occasionally,

Chapter | 16 |

Figure 16-7  Cellulitis involving the submental and submandibular
region. The cellulitis is indurated on palpation, and the patient is sick.
(From Flynn TR: Surgical management of orofacial infections. Atlas Oral
Maxillofac Surg Clin North Am 8:79, 2000.)

Figure 16-8  Well-localized abscess with fluctuance in the center and
induration at its periphery. (Courtesy of Richard G. Topazian, DDS.)

however, extraoral radiographs such as a panoramic radiograph may
be necessary because of limited mouth opening, tenderness, or other
extenuating circumstances.
After the physical examination, the practitioner should begin to
have a sense of the stage of the presenting infection. Very soft, mildly
tender, edematous swellings indicate the inoculation stage, whereas
an indurated swelling indicates the cellulitis stage (Fig. 16-7), and
central fluctuance indicates an abscess (Fig. 16-8). Soft tissue infections in the inoculation stage may be cured by removal of the odontogenic cause, with or without supportive antibiotics; infections in
the cellulitis or abscess stages require removal of the dental cause of
infection plus incision and drainage and antibiotics.
Distinctions between the inoculation, cellulitis, and abscess stages
are typically related to duration, pain, size, peripheral definition and
consistency on palpation, presence of purulence, infecting bacteria,
and potential danger (see Table 16-3). The duration of cellulitis is
usually thought to be acute and is the most severe presentation of
infection. An abscess, however, is a sign of increasing host resistance
to infection. Cellulitis is usually described as being more painful than

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Part | IV |

Infections

an abscess, which may be the result of its acute onset and tissue
distention.
Edema, the hallmark of the inoculation stage, is typically diffuse
and jelly-like, with minimal tenderness to palpation. The size of a
cellulitis is typically larger and more widespread than that of an
abscess or edema. The periphery of a cellulitis is usually indistinct,
with a diffuse border that makes it difficult to determine where the
swelling begins or where it ends. The abscess usually has distinct and
well-defined borders. Consistency to palpation is one of the primary
distinctions among the stages of infection. When palpated, edema
can be very soft or doughy; a severe cellulitis is almost always
described as indurated or even as being “boardlike.” The severity of
the cellulitis increases as its firmness to palpation increases. On palpation, an abscess feels fluctuant because it is a pus-filled tissue cavity.
Thus, an infection may appear innocuous in its early stages and
extremely dangerous in its more advanced, indurated, rapidly spreading stages. A localized abscess is typically less dangerous because it
is more chronic and less aggressive.
The presence of pus usually indicates that the body has locally
walled off the infection and that the local host resistance mechanisms
are bringing the infection under control. In many clinical situations,
the distinction between severe cellulitis and abscess may be difficult
to make, especially if an abscess lies deeply within the soft tissue. In
some patients, an indurated cellulitis may have areas of abscess formation within it (see Chapter 17).
Severe infections occupying multiple deep fascial spaces may be

in an early stage in one anatomic space, and in a more severe, rapidly
progressive stage in another fascial space. A severe, deeply invading
infection may pass through ever deeper anatomic spaces in a predictable fashion, similar to a house fire, where smoke may be present in
one room, intense heat in another, and open flames near the source
of the fire. The goal of therapy in such infections is to abort the spread
of the infection in all involved anatomic spaces. These infections are
discussed in detail in Chapter 17.
In summary, edema represents the earliest inoculation stage of
infection which is most easily treated. Cellulitis is an acute, painful
infection with more swelling and diffuse borders. Cellulitis has a hard
consistency on palpation and contains no visible pus. Cellulitis may
be a rapidly spreading process in serious infections. An acute abscess
is a more mature infection with more localized pain, less swelling,
and well-circumscribed borders. The abscess is fluctuant on palpation
because it is a pus-filled tissue cavity. A chronic abscess is usually slow
growing and less serious than cellulitis, especially if the abscess has
drained spontaneously to the external environment.

Principle 2: Evaluate State of Patient’s Host
Defense Mechanisms
Part of the evaluation of the patient’s medical history is designed to
estimate the patient’s ability to defend against infection. Several
disease states and several types of drug use may compromise this
ability. Immunocompromised patients are more likely to have infections, and these infections often become serious more rapidly. Therefore, to manage their infections more effectively, it is important to be
able to identify those patients who may have compromised host
defenses.
Medical conditions that compromise host defenses.  Delineation of those medical conditions that may result in decreased host
defenses is important. These compromises allow more bacteria to
enter the tissues or to be more active, or they prevent the humoral
or cellular defenses from exerting their full effect. Several specific

conditions may compromise patients’ defenses (Box 16-1).
Uncontrolled metabolic diseases—such as uncontrolled diabetes,
end-stage renal disease with uremia, and severe alcoholism with

302

Box 16-1  Compromised Host Defenses

Uncontrolled Metabolic Diseases
•
•
•
•

Poorly controlled diabetes
Alcoholism
Malnutrition
End-stage renal disease

Immune System–Suppressing Diseases
• Human immunodeficiency virus/acquired immunodeficiency
syndrome
• Lymphomas and leukemias
• Other malignancies
• Congenital and acquired immunologic diseases

Immunosuppressive Therapies
• Cancer chemotherapy
• Corticosteroids
• Organ transplantation

malnutrition—result in decreased function of leukocytes, including
decreased chemotaxis, phagocytosis, and bacterial killing. Of these
metabolic diseases, poorly controlled type 1 (insulin-dependent) and
type 2 (non–insulin-dependent) diabetes are the most common
immunocompromising diseases, and worsening control of hyperglycemia correlates directly with lowered resistance to all types of
infections.
The second major group of immunocompromising diseases
includes those that interfere with host defense mechanisms, for
example, leukemias, lymphomas, and many types of cancer. These
diseases result in decreased white cell function and decreased antibody synthesis and production.
Human immunodeficiency virus (HIV) infection attacks T
lymphocytes, affecting a person’s resistance to viruses and other
intracellular pathogens. Fortunately, odontogenic infections are
caused largely by extracellular pathogens (bacteria). Therefore, HIVseropositive individuals are able to combat odontogenic infections
fairly well until acquired immunodeficiency syndrome (AIDS) has
progressed to advanced stages, when B lymphocytes are also severely
impaired. Nonetheless, care for the HIV-seropositive patient with an
odontogenic infection is usually more intensive than for the otherwise healthy patient.
Pharmaceuticals that compromise host defenses.  Patients
taking certain drugs are also immunologically compromised. Cancer
chemotherapeutic agents can decrease circulating white cell counts
to low levels, commonly less than 1000 cells per milliliter (cells/mL).
When this occurs, patients are unable to defend themselves effectively
against bacterial invasion. Patients receiving immunosuppressive
therapy, usually for organ transplantation or autoimmune diseases,
are compromised. The common drugs in these categories are cyclosporine, corticosteroids, tacrolimus (Prograf), and azathioprine
(Imuran). These drugs decrease the function of T and B lymphocytes
and immunoglobulin production. Thus, patients taking these medications are more likely to have severe infections. The immunosuppressive effects of some cancer chemotherapeutic agents can last for
up to a year after therapy ends.

In summary, when evaluating a patient whose chief complaint
may be an infection, the patient’s medical history should be carefully
reviewed for the presence of diabetes, severe renal disease, alcoholism
with malnutrition, leukemias and lymphomas, cancer chemotherapy,
and immunosuppressive therapy of any kind. When the patient’s
history includes any of these, the patient with an infection must be
treated much more vigorously because the infection may spread more


Principles of Management and Prevention of Odontogenic Infections

Box 16-2  Criteria for Referral to an Oral-Maxillofacial
Surgeon
•
•
•
•
•
•
•
•
•
•

Difficulty breathing
Difficulty swallowing
Dehydration
Moderate to severe trismus (interincisal opening less
than 20 mm)
Swelling extending beyond the alveolar process

Elevated temperature (greater than 101°F)
Severe malaise and toxic appearance
Compromised host defenses
Need for general anesthesia
Failed prior treatment

rapidly. Referral to an oral-maxillofacial surgeon for early and aggressive surgery to remove the cause and initiate parenteral antibiotic
therapy must be considered.
Additionally, when a patient with a history of one of these problems is seen for routine oral surgical procedures, it may be necessary
to provide the patient with prophylactic antibiotic therapy to decrease
the risk of postoperative wound infection. Use of the guidelines and
regimens for prevention of endocarditis published by the American
Heart Association (AHA) and American Dental Association (ADA) is
a practical way to manage this problem.

Principle 3: Determine Whether Patient
Should Be Treated by General Dentist or
Oral-Maxillofacial Surgeon
Most odontogenic infections seen by the dentist can be managed
with the expectation of rapid resolution. Odontogenic infections,
when treated with minor surgical procedures and antibiotics, if indicated, almost always respond rapidly. However, some odontogenic
infections are potentially life threatening and require aggressive
medical and surgical management. In these special situations, early
recognition of the potential severity is essential, and these patients
should be referred to an oral-maxillofacial surgeon for definitive
management. As the specialist with the best training and experience
in the management of severe odontogenic infections, the oralmaxillofacial surgeon can optimize the outcomes and minimize the
complications of these infections. For some patients, hospitalization
is required, whereas others can be managed as outpatients.
When a patient with an odontogenic infection comes for treatment, the dentist must have a set of criteria by which to judge the

seriousness of the infection (Box 16-2). If some or all of these criteria
are met, immediate referral must be considered.
Three main criteria indicate immediate referral to a hospital emergency room because of an impending threat to the airway. The first
criterion is a history of a rapidly progressing infection. This means
that the infection began 1 or 2 days before the interview and is
growing rapidly worse, with increasing swelling, pain, and other
associated signs and symptoms. This type of odontogenic infection
may cause swelling in deep fascial spaces of the neck, which can
compress and deviate the airway. The second criterion is difficulty
breathing (dyspnea). Patients who have severe swelling of the soft
tissue of the upper airway as the result of infection may have difficulty
maintaining a patent airway. In these situations, the patient often will
refuse to lie down, have muffled or distorted speech, and be obviously distressed by breathing difficulties. This patient should be
referred directly to an emergency room because immediate surgical
attention may be necessary to maintain an intact airway. The third

Chapter | 16 |

urgent criterion is difficulty swallowing (dysphagia). Patients with
acutely progressive deep fascial space infections may also have difficulty swallowing their saliva. Drooling is an ominous sign because
the inability to control one’s secretions frequently indicates a narrowing of the oropharynx and the potential for acute airway obstruction.
This patient should also be transported to the hospital emergency
room immediately because surgical intervention or intubation may
be required for airway maintenance. Definitive treatment of the infection can follow once the airway is secure.
Several other criteria should indicate referral to an oralmaxillofacial surgeon. Patients who have extraoral swellings such as
buccal space infections or submandibular space infections may
require extraoral surgical incision and drainage (I&D) as well as
hospitalization. Next, although infection frequently causes an elevated temperature, a temperature higher than 101°F indicates a
greater likelihood of severe infection, and this patient should be
referred to the hospital. Another important sign is trismus, the inability to open the mouth widely. In odontogenic infections, trismus

results from the involvement of the muscles of mastication by the
inflammatory process. Mild trismus can be defined as a maximum
interincisal opening between 20 and 30 mm; moderate trismus is an
interincisal opening between 10 and 20 mm; and severe trismus is
an interincisal opening of less than 10 mm.
Moderate or severe trismus may be an indication of the spread of
the infection into the masticator space (surrounding the muscles of
mastication) or, worse, either or both the lateral pharyngeal space
and the retropharyngeal space surrounding the pharynx and the
trachea. In this situation, referral to a specialist is necessary for evaluation of upper airway patency. In addition, systemic involvement of
an odontogenic infection is an indication for referral. Patients with
systemic involvement have a typical toxic facial appearance: glazed
eyes, open mouth, and a dehydrated, sick appearance. When this is
seen, the patient is usually fatigued, has a substantial amount of pain,
has an elevated temperature, and is dehydrated. Finally, if the patient
has compromised host defenses, he or she may have to be hospitalized. An oral-maxillofacial surgeon is qualified to admit the patient
expeditiously to the hospital for definitive care.
In summary, within the first few minutes of the initial patient
encounter, the three principles mentioned above allow the dentist to
assess the severity of the infection, evaluate host defenses, and expeditiously decide on the best setting for the patient’s care. In doubtful
situations, it is always best to err on the side of caution and refer the
patient for a higher level of care. Appropriate decision making at this
stage can prevent serious morbidity and the occasional mortality that
still occur because of odontogenic infections.

Principle 4: Treat Infection Surgically
The primary principle of management of odontogenic infections is
to perform surgical drainage and to remove the cause of the infection.
Surgical treatment may range from something as straightforward as
an endodontic access opening and extirpation of the necrotic tooth

pulp to treatment as complex as the wide incision of the soft tissue
in the submandibular and neck regions for a severe infection or even
open drainage of the mediastinum.
The primary goal in surgical management of infection is to remove
the cause of the infection, which is most commonly a necrotic pulp
or deep periodontal pocket. A secondary goal is to provide drainage
of accumulated pus and necrotic debris.
When a patient has a typical odontogenic infection, the most
likely appearance is a carious tooth with a periapical radiolucency
and a small vestibular abscess. With this presentation, the dentist has
the following surgical options: endodontic treatment or extraction,
with or without I&D. If the tooth is not to be extracted, it should be
opened and its pulp removed, which results in elimination of the

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Part | IV |

Infections

cause and limited drainage through the apical foramen of the tooth.
If the tooth cannot be salvaged or is not restorable, it should be
extracted as soon as possible.
Extraction provides removal of the cause of the infection and drainage of the accumulated periapical pus and debris. In addition to the
endodontic procedure or extraction of the tooth, an I&D procedure
may be required for an infection that has spread beyond the periapical
region. Incision of the abscess or cellulitis allows removal of the accumulated pus and bacteria from the underlying tissue. Evacuation of the
abscess cavity dramatically decreases the load of bacteria and necrotic
debris. Evacuation also reduces the hydrostatic pressure in the region

by decompressing tissues, which improves the local blood supply and
increases the delivery of host defenses and antibiotics to the infected
area. I&D of a cellulitis serves to abort the spread of the infection into
deeper anatomic spaces. The I&D procedure includes the insertion of
a drain to prevent premature closure of the mucosal incision, which
could allow the abscess cavity to re-form. It is important to remember
that the surgical goal is to achieve adequate drainage. If endodontic
opening of the tooth does not provide adequate drainage of the
abscess, it is essential to perform an I&D.
The technique for I&D of a vestibular abscess or cellulitis is straightforward (Fig. 16-9). The preferred site for intraoral incision is directly
over the site of maximum swelling and inflammation. However, it is
important to avoid incising across a frenum or the path of the mental
nerve in the lower premolar region. When I&D procedures are performed extraorally, a more complex set of criteria must be met when
selecting a site for the incision. Once the area of incision has been
selected, a method of pain control must be used. Regional nerve block
anesthesia is preferred when it can be achieved by injecting in an
area away from the site of infection. Alternatively, infiltration of local

A

anesthetic solution into and around the area to be drained can be
performed. Once the local anesthetic needle has been used in an
infected site, it should not be reused in an uninfected area.
Before the actual incision of the abscess is performed, obtaining a
specimen for culture and sensitivity (C&S) testing must be considered.
If the decision is made to perform a culture, it is carried out as the
initial portion of the surgery (Box 16-3). After the site of surgery has
been anesthetized, the surface mucosa is disinfected with a solution
such as povidone-iodine (Betadine) and dried with sterile gauze. A
large-gauge needle, usually 18 gauge, is used for specimen collection.

A small syringe, usually 3 mL, is adequate. The needle is then inserted
into the abscess or cellulitis, and 1 or 2 mL of pus or tissue fluid is
aspirated. The specimen may contain only tissue fluid and blood
instead of pus, yet it commonly provides sufficient bacteria for an
accurate culture. The specimen is then inoculated directly into aerobic
and anaerobic culturettes, which are sterile tubes containing a swab
and bacterial transport medium. Culturettes and specimen bottles that
are appropriate for both aerobes and anaerobes are also available. All

Box 16-3  Indications for Culture and Antibiotic
Sensitivity Testing
•
•
•
•
•
•

C

B

D

Infection spreading beyond the alveolar process
Rapidly progressive infection
Previous, multiple antibiotic therapy
Nonresponsive infection (after more than 48 hours)
Recurrent infection
Compromised host defenses

E

Figure 16-9  A, Periapical infection of lower premolar extends through buccal plate and creates sizable vestibular abscess. B, Abscess is incised with
No. 11 blade. C, Beaks of hemostat are inserted through incision and opened so that beaks spread to break up any loculations of pus that may exist
in abscessed tissue. D, A small drain is inserted to depths of abscess cavity with a hemostat. E, The drain is sutured into place with a single black silk
suture. Note that pus usually flows out along, rather than through, a tubular drain.

304


Principles of Management and Prevention of Odontogenic Infections
culturettes and specimen bottles have a limited shelf-life, so the expiration date should be checked before use. Care must be taken to keep the
anaerobic culture tube fully upright while open to prevent the escape
of the carbon dioxide that is needed to maintain the tube’s anaerobic
environment. As discussed before, anaerobic bacteria are almost
always present in odontogenic infections, so care must be taken to
provide the laboratory with the best specimen to find them. The
surgeon should request, in writing, a gram stain, aerobic and anaerobic cultures, and antibiotic sensitivity testing.
Once the culture specimen is obtained, an incision is made with
a scalpel blade just through the mucosa and submucosa into the
abscess cavity (see Fig. 16-9). The incision should be short, usually
no more than 1 cm in length. Once the incision is completed, a
closed curved hemostat is inserted through the incision into the
abscess cavity. The hemostat is then opened in several directions to
break up any small loculations (cavities of pus) that have not been
opened by the initial incision. Any pus or tissue fluid that drains out
during this time should be aspirated into the suction and should not
be allowed to drain into the patient’s mouth. If, however, an adequate
specimen has not been obtained with aspiration, aerobic and anaerobic culturette swabs may be carefully introduced into the wound

without contaminating the swabs on the surface mucosa. Adequate
specimens can be obtained in this manner, even if obvious pus is not
present in the wound.
Once all areas of the abscess cavity have been opened and all pus
has been removed, a small drain is inserted to maintain the opening.
The most commonly used drain for intraoral abscesses is a quarterinch sterile Penrose drain. A frequently used substitute is a small strip
of sterilized rubber dam or surgical glove material. Take care to note
any patient sensitivity to latex when selecting the drain material. A
piece of drain of adequate length to reach the depth of the abscess
cavity is prepared and inserted into the cavity using a hemostat. The

Chapter | 16 |

drain is then sutured to one edge of the incision with a nonresorbable
suture. The suture should be placed in viable tissue to prevent loss
of the drain because it might tear through friable, nonvital tissue.
The drain should remain in place until all the drainage has
stopped, usually for 2 to 5 days. Removal is done by simply cutting
the suture and slipping the drain from the wound.
Inoculation-stage infections, that initially appear as edema with a
soft, doughy, diffuse, mildly tender swelling, do not typically require
I&D. Surgical management of infections of this type is limited to
removal of the necrotic pulp or removal of the involved tooth.
Adjunctive antibiotic therapy may be used, according to the indications discussed below.
It is critical to keep in mind that the primary method for treating
odontogenic infections is to perform surgery to remove the source of
the infection and drain the anatomic spaces affected by indurated
cellulitis or an abscess. Whenever an abscess or cellulitis is diagnosed,
the surgeon must drain it. Failure to do so may result in worsening
of the infection and failure of the infection to resolve, even if antibiotics are given. Even if the tooth cannot be immediately opened or

extracted, an I&D should be done.
Some clinicians believe that I&D of a cellulitis may allow the
infection to spread into deeper tissues by opening them up to infecting bacteria. The experience of others has shown that establishing
drainage for a cellulitis serves to abort the spread of infection. In a
prospective study of 37 patients hospitalized for severe odontogenic
infection, approximately 25% of the cases had drainage in the cellulitis stage. On multivariate analysis, the stage of infection had no
significant effect on complications or the length of hospital stay.
The algorithm presented in Figure 16-10 is a decision pathway for
the management of uncomplicated odontogenic infections, which
follows the principles described in this chapter. After deciding to treat
the patient in the outpatient setting, the dentist should determine
Follow-up
preventive and
restorative care

History and
physical examination
pain
swelling
caries
periodontitis
pericoronitis

Odontogenic
infection

Inoculation
stage

Assess Severity

airway compromise
anatomic location
rate of progression
Evaluate Host Defenses
medical comorbidities
immune compromise
systemic reserve

X-ray examination
periapical pathosis
periodontal bone loss
impacted tooth

Outpatient
therapy

Cellulitis or
abscess stage

Remove dental cause
extraction
endodontics
débridement

Improvement
by 72h
Œtemperature
Œfever
Œswelling

Oral antibiotics
supportive care
control systemic disease
hydration, nutrition

Incision and drainage

Failure to
improve by
72h

Remove dental cause
extraction
endodontics
débridement

Referral to
oral and
maxillofacial
surgeon
Figure 16-10  Management algorithm for odontogenic infections. (Data from Flynn TR: Deep fascial space infections. In Laskin DM, Abubaker AO,
editors: Decision making in oral and maxillofacial surgery, Chicago, IL, 2007, Quintessence.)

305


Part | IV |

Infections

whether the infection is in the inoculation (edema) stage or if it has
progressed to cellulitis or an abscess. In the inoculation stage, the
dental cause of the infection should be treated surgically. An antibiotic may also hasten resolution of the infection at this stage. If the
infection has progressed to cellulitis or an abscess, then an I&D and
the appropriate dental therapy should be performed. Sometimes, a
separate I&D is not necessary if the abscess cavity drains completely
through an extraction socket. Antibiotic therapy should be used when
complete abscess drainage cannot be achieved by extraction alone.
The criteria for referral to an oral-maxillofacial surgeon are
listed in Box 16-2. In summary, in the presence of potential or actual
airway compromise, spread of infection beyond the alveolar process,
medical or immune system compromise, or signs of systemic in­
volvement, immediate referral to an oral-maxillofacial surgeon or, in
life-threatening cases, referral to a hospital emergency room, is
indicated.

Principle 5: Support Patient Medically
A patient’s systemic resistance to infection is perhaps the most important determinant of a good outcome. Host systemic resistance must
be considered in three areas: (1) immune system compromise, (2)
control of systemic diseases, and (3) physiologic reserves.
Diseases that compromise the immune system are listed in Box
16-1. Odontogenic infections that occur in patients with immune
system compromise should be treated by a specialist. Often, hospitalization and medical consultation are required. The treatment team
selects therapies designed to enhance the immune response, combat
the infection medically with bactericidal antibiotics, and optimize
surgical management of the infection.
Many systemic diseases also reduce the ability of the patient to
resist infection and to undergo treatment. In diabetes, for example,
the control of blood sugar is directly correlated with resistance to
infection. Host response to a significant infection increases the blood

sugar levels and, therefore, the insulin requirements of a person with
diabetes. Moreover, cardiovascular diseases decrease the ability of the
host to respond to the stress of infection and surgery. Therefore,
optimizing control of hypertension, cardiac dysrhythmias, and atherosclerotic heart disease is an essential part of the comprehensive
management of odontogenic infections. Medications may also affect
the treatment of odontogenic infections. For example, the patient
receiving anticoagulant therapy with warfarin (Coumadin) may need
reversal of anticoagulation before surgery can be safely performed.
Patients with systemic conditions, especially of the immune, cardiovascular, respiratory, hematologic, and metabolic systems, often need
sophisticated medical support from a team of specialists.
Even patients without medically compromising diseases may
have reduced or altered physiologic reserves to draw on as they
combat an odontogenic infection. Children, for example, are particularly susceptible to dehydration and high fevers. Elderly patients,
however, are less able to mount a fever but are susceptible to dehy­
dration. Fever increases daily fluid requirements in the adult by about
800 mL/°F/day, and daily caloric requirements by 3% to 5% per
degree Fahrenheit per day. However, temperatures up to 103°F may
be beneficial in combating infections. Therefore, judicious control of
highly elevated fever, along with active hydration and nutritional
support, are important components of the management of odontogenic infections.
Because of pain, difficulty swallowing, or both, patients frequently
have not had adequate fluid intake, nutritional intake, or rest. During
the immediate post-treatment period, patients should be encouraged
to drink sufficient water or juice so that they urinate regularly and to
take high-calorie nutritional supplements. Patients should also be
prescribed adequate analgesics for relief of pain to help them rest.
Patients should be given careful postoperative instructions, and they

306

should be able to manage their self-care. The clinician is responsible
to ensure that patients are provided careful instructions about these
important issues.

Principle 6: Choose and Prescribe
Appropriate Antibiotic
The appropriate antibiotic for treating an odontogenic infection must
be chosen carefully. After weighing all factors, the clinician may
decide that no antibiotic is necessary at all; in other situations, broadspectrum or even combination antibiotic therapy may be indicated.
A variety of factors must be considered when choosing an antibiotic
from the nearly 70 antibiotics currently available. Antibiotics must
be viewed as a double-edged sword. Although appropriate use may
result in dramatic resolution of infections and cure, misuse of antibiotics provides little benefit to offset the associated risks and expense
of antibiotic administration. Studies have shown that even the
administration of oral penicillin promotes the growth of penicillinresistant organisms in the oropharyngeal flora of the patient, the
patient’s family, and even the patient’s coworkers or classmates.
Therefore, the following guidelines are recommended for consideration when choosing a specific antibiotic.
Determine the need for antibiotic administration.  A common
misconception is that all infections, by definition, require antibiotic
administration. This is not necessarily the case. In some situations,
antibiotics are not useful and may even be contraindicated. In making
this determination, three factors must be considered: (1) The first
factor is the seriousness of the infection when the patient comes to
the dentist. If the infection has caused swelling, has progressed
rapidly, or is diffuse cellulitis, evidence supports the use of antibiotics
in addition to surgical therapy. (2) The second consideration is
whether adequate surgical treatment can be achieved. In many situations, extraction of the offending tooth may result in rapid resolution of the infection. Contrary to widely held opinion, extraction of
a tooth in the presence of infection does not promote the spread of
infection. Several studies have shown that removal of a tooth in the
presence of infection hastens the resolution and minimizes the complications of the infection, such as time out of work, hospitalization,

and the need for extraoral I&D. Therefore, prompt removal of the
offending tooth (or teeth) in the presence of infection is to be encouraged; a prior period of antibiotic therapy is not necessary. Moreover,
when surgery cannot be done immediately, a course of antibiotics
does not reliably prevent worsening of the infection. In a blinded
study of 130 patients presenting to a hospital emergency room with
toothache, no significant difference was seen in the progression of
infection between the placebo and the antibiotic groups. Only the
presence of a restoration and a periapical lesion larger than 2 mm
predicted subsequent development of spreading infection. (3) The
third consideration is the state of the patient’s host defenses. A young,
healthy patient may be able to mobilize host defenses and may not
need antibiotic therapy for resolution of a minor infection. However,
patients who have any type of decreased host resistance, such as those
with severe metabolic disease or those receiving cancer chemo­
therapy, may require vigorous antibiotic therapy even for minor
infections.
When these three factors are balanced, several definite indications
for antibiotic use in dentistry become clear (Box 16-4). The first
and most common indication is the presence of an acute-onset infection
with diffuse swelling and moderate-to-severe pain. This infection is
usually in the cellulitis stage; and with appropriate antibiotic therapy,
I&D, and treatment of the offending tooth, rapid resolution is
expected. The second indication is almost any type of infection in a
patient who is immunologically compromised. Such patients who have
infections of any severity should be considered candidates for


Principles of Management and Prevention of Odontogenic Infections

Box 16-4  Indications for Therapeutic Use of Antibiotics

•
•
•
•
•
•
•

Swelling extending beyond the alveolar process
Cellulitis
Trismus
Lymphadenopathy
Temperature higher than 101°F
Severe pericoronitis
Osteomyelitis

Box 16-5  Situations in Which Use of Antibiotics Is
Not Necessary
•
•
•
•
•
•

Patient demand
Severe pain
Toothache
Periapical abscess
Dry socket

Multiple dental extractions in a patient who is not
immunocompromised
• Mild pericoronitis (inflammation of the operculum only)
• Drained alveolar abscess

antibiotic administration. The third indication for antibiotic therapy
is the presence of an infection that has progressed to involvement
of the deep fascial spaces. In these situations, the infection is aggressive
enough to have spread beyond the alveolar process of the jaws,
indicating that the host defenses are inadequate to contain the infection. The fourth indication is severe pericoronitis, with temperatures
higher than 100°F, trismus, and swelling of the lateral aspect of the
face, which occurs most commonly around impacted mandibular
third molars. Finally, the patient who has osteomyelitis requires
antibiotic therapy in addition to surgery to achieve resolution of
the infection.
On the basis of the same criteria, antibiotic therapy is not indicated and is even contraindicated in other situations (Box 16-5). The
first is a minor, chronic, well-localized abscess, in which case, extraction
of the offending tooth results in complete evacuation of a periapical
abscess, provided that the patient’s host defenses are intact and that
the patient has no other immunocompromising conditions. An
example of this is the patient without symptoms and who may
require the extraction of teeth with chronic periapical abscesses, a
draining parulis, or severe periodontitis. A second, similar contraindication is a well-localized dentoalveolar abscess, with little or no facial
swelling. In these situations, endodontic therapy can be performed,
or the tooth can be extracted along with I&D of the swelling on the
alveolar process, which will result in rapid resolution in most patients.
Third is a localized alveolar osteitis (dry socket). Treatment of the dry
socket is primarily palliative, and dry socket is not treated as an infection. Although bacterial pathogens may play a role in the etiology of
a dry socket, the clinical problem of alveolar osteitis is self-limiting
and appears to be caused by premature fibrinolysis (dissolution of a

blood clot). Fourth, patients who have mild pericoronitis with minor
gingival edema and mild pain do not require antibiotics for resolution
of their infection. Irrigation with hydrogen peroxide or chlorhexidine, plus extraction of the partially erupted tooth will result in resolution. Antibiotics should not be prescribed simply because a patient
demands them for a routine toothache or for dental extractions in a
patient without any immune system compromise.

Chapter | 16 |

Box 16-6  Effective Orally Administered Antibiotics
Useful for Odontogenic Infections
•
•
•
•
•
•

Penicillin
Amoxicillin
Clindamycin
Azithromycin
Metronidazole
Moxifloxacin

In summary, antibiotics should be used when clear evidence exists
of bacterial invasion into deeper tissues that is greater than the host
defenses can overcome. Patients who have an impaired ability to
defend themselves against infection and patients who have infections
that are not immediately amenable to surgical treatment should be
considered for antibiotic therapy. Antibiotics should not be used

when no evidence of bacterial invasion of deeper tissues is found.
Antibiotics do not hasten wound healing and do not provide any
benefit for nonbacterial (e.g., viral) conditions. Patients who have
inflammatory pulpitis have severe pain, but the pain results from the
local inflammatory reaction within the pulp, not from bacterial infection spreading into deeper tissues. These patients should not routinely be given antibiotic therapy.
Use empirical therapy routinely.  Odontogenic infections are
caused by a highly predictable group of bacteria, and the antibiotic
sensitivity of these organisms is well known and consistent. As a
result, the use of culture and sensitivity (C&S) testing is not necessary
for routine odontogenic infections. The bacteria that cause odontogenic infections are overwhelmingly facultative oral streptococci;
anaerobic streptococci, including Parvimonas micra (formerly Pepto­
streptococcus micros); and Prevotella and Fusobacterium species. Other
species of bacteria may also be cultured from these infections, but
they appear to be opportunistic rather than causative. Fortunately, the
antibiotic susceptibility of causative bacteria is fairly predictable.
Orally administered antibiotics that are effective against odontogenic
infections include penicillin, amoxicillin, clindamycin, azithromycin,
metronidazole, and moxifloxacin (Box 16-6). A recent systematic
review of randomized clinical trials comparing penicillin or amoxicillin with newer antibiotics found that when appropriate dental surgery
was done, none of newer antibiotics had a significantly greater clinical cure rate than amoxicillin or penicillin.
The antibiotics mentioned above (except metronidazole) are
effective against aerobic and facultative streptococci, and oral anaerobes. Metronidazole is effective only against obligate anaerobic bacteria, but the effectiveness of this antibiotic class in odontogenic
infections has been shown in a prospective study. Several important
variations can be found among these antibiotics. (See Appendix VI
for a detailed description of the various antibiotics.)
Because the microbiology and antibiotic sensitivity of oral pathogens are well known, it is a reasonable therapeutic maneuver to use
one of these antibiotics empirically, that is, administer the antibiotic
on the assumption that it is the appropriate drug. The drug of choice
is usually penicillin. Alternative drugs for use in penicillin-allergic
patients are clindamycin and azithromycin. Metronidazole is useful

only against anaerobic bacteria and should be reserved for a situation
in which only anaerobic bacteria are identified, in combination with
an antibiotic that has antiaerobic activity, such as penicillin, or when
other antibiotics are contraindicated.
Clearly, patients frequently fail to take the medication correctly
as prescribed. In fact, Socrates, in 400 bc, cautioned physicians to
be aware that patients will lie about taking their prescribed
medications.

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Part | IV |

Infections

Reliable data from many studies demonstrate that patient compliance decreases with increasing numbers of pills per day. When it is
necessary to take the prescription once daily, patient compliance is
approximately 80%. However, when it is necessary to take the pill
two times daily, compliance decreases to 69%, and drops even further
to 35% for four times daily. Therefore, if the clinician has a reasonable choice, he or she should prescribe antibiotics that need to be
taken the fewest times daily to improve patient compliance.
For example, amoxicillin and clindamycin are usually taken three
times daily instead of four times daily (as is penicillin). Azithromycin
is taken twice a day, instead of four times daily (as is erythromycin).
Moxifloxacin is taken once daily. Thus, when other important factors
such as antibacterial effectiveness, side effects, drug interactions, and
cost are reasonably equal, a drug that needs to be taken less frequently is preferable. As discussed subsequently, however, significant
differences exist among these antibiotics in their side effects, drug
interactions, and cost.

Routine C&S testing is not cost-effective in the treatment of
routine odontogenic infections. However, in some cases, the dentist
should seriously consider sending a specimen for C&S testing (see
Box 16-3). The first case is the rapid onset of severe infection and its
rapid spread. Delay in bacterial identification may have disastrous
consequences in this situation; therefore, culturing early in the clinical course is indicated. The second case is postoperative infection. If
a patient had no signs of infection when the original surgery was
done but returns 3 or 4 days later with an infection, the chances of
nonindigenous bacteria causing the infection are higher. Precise identification of the causative bacteria early on may facilitate the timely
administration of the appropriate antibiotic and, thus, the resolution
of the infection. The third case is an infection that does not resolve
as expected. In these situations, the clinician should make every effort
to obtain a specimen of pus or tissue fluid for C&S testing. The fourth
case is a recurrent infection. When the initial infectious problem has
resolved and an infection-free period of 2 days to 2 weeks followed
by a second infection occurs, the probability is high that the infection
is caused by bacteria that are resistant to the previously used antibiotic. The fifth case is the patient who has compromised host defenses.
Patients with immune system compromise have a propensity to
harbor unusual pathogens that can be identified by C&S testing.
In the foreseeable future, conventional C&S testing may be
replaced by molecular methods that are currently used only in
research. Bacteria can be identified even after they die from their
genetic material, using the polymerase chain reaction to amplify tiny
amounts of bacterial deoxyribonucleic acid (DNA) and ribonucleic
acid (RNA). Single-stranded nucleic acids from an unknown sample
can be hybridized to single-stranded genes from known species,
which would lead to a positive identification of infecting bacteria.
These methods have identified the involvement of a large number of
unculturable pathogens in odontogenic infections, the presence of
which was only suspected in the past. In the future, these methods

may be able to detect antibiotic-resistance genes directly as well,
which would make it possible to provide a prompt diagnosis of the
infecting species and their antibiotic sensitivity patterns.
Use the narrowest-spectrum antibiotic.  When an antibiotic is
administered to a patient, most of the susceptible bacteria are killed.
If the antibiotic is a narrow-spectrum antibiotic, it kills bacteria of a
narrow range. For example, penicillin will kill streptococci and oral
anaerobic bacteria but will have little effect on the staphylococci of
the skin and almost no effect on gastrointestinal (GI) tract bacteria.
As a result, penicillin has little or no effect on the GI tract and does
not facilitate a multitude of other bacteria developing resistance. By
contrast, drugs such as amoxicillin-clavulanate (Augmentin) are
broad-spectrum antibiotics, inhibiting not only streptococci and oral
anaerobes but also a variety of staphylococci and enteric gramnegative rods. Thus, when this antibiotic is given, it has an effect on

308

Box 16-7  Narrow-Spectrum and Broad-Spectrum
Antibiotics

Narrow-Spectrum Antibiotics Useful for Treating
Simple Odontogenic Infections
•
•
•
•

Penicillin
Amoxicillin
Clindamycin

Metronidazole

Broad-Spectrum Antibiotics Useful for Treating
Complex Odontogenic Infections
•
•
•
•

Amoxicillin with clavulanic acid (for sinus infections)
Azithromycin
Tetracycline
Moxifloxacin

Box 16-8  Simple and Complex Odontogenic Infections

Simple Odontogenic Infections
• Swelling limited to the alveolar process and vestibular space
• First attempt at treatment
• Patient who is not immunocompromised

Complex Odontogenic Infections
• Swelling extending beyond the vestibular space
• Failed prior treatment
• Immunocompromised patient

skin and GI bacteria, which may result in problems caused by alterations of host flora and overgrowth of resistant bacteria. In addition,
broad-spectrum antibiotics enable a multitude of bacteria to develop
resistance, and this resistance can be passed on by dental patients to
their families, coworkers, and entire communities.

The ADA’s Council on Scientific Affairs has issued guidelines,
which are based on a review of the available scientific literature,
recommending that dentists use only narrow-spectrum antibiotics to
treat simple infections. A list of narrow-spectrum and broad-spectrum
antibiotics is provided in Box 16-7. Broad-spectrum antibiotics may
be used for complex infections, which are not defined in the ADA
advisory statement. Nonetheless, a simple odontogenic infection can
be defined as one involving only the alveolar process or the oral
vestibule, in its first course of treatment, and in an immunocompetent individual. A complex infection may be defined as one that has
spread beyond the alveolar process and oral vestibule, with prior
treatment failures, or in an immunocompromised patient. The characteristics of simple and complex odontogenic infections are differentiated in Box 16-8.
In summary, antibiotics that have narrow-spectrum activity against
causative organisms are just as effective as antibiotics that have broadspectrum activity, but without upsetting normal host microflora
populations and increasing the chances of bacterial resistance. With
appropriate surgery, an appropriate choice can be made from among
the commonly used antibiotics on the basis of safety, cost, and the
medical history of the patient.
Use the antibiotic with the lowest incidence of toxicity and
side effects.  Most antibiotics have a variety of toxicities and side
effects that limit their usefulness. These range from mild ones to side
effects that are so severe that the antibiotic causing them cannot be
used in clinical practice. The older-generation antibiotics usually used
for odontogenic infections have a surprisingly low incidence of


Principles of Management and Prevention of Odontogenic Infections
toxicity-related problems. The newer-generation antibiotics, however,
may have significant toxicities and drug interactions. Therefore, it is
becoming increasingly important for the clinician to understand the
toxicities, side effects, and drug interactions of the drugs he or she

may prescribe.
Allergy is the major side effect of penicillin. Approximately 2% or
3% of the total population is allergic to penicillin. Patients who have
allergic reactions to penicillin, as exhibited by hives, itching, or
wheezing, should not be given penicillin again. Penicillin does not
have other major side effects or toxicities in the normal dose range
used by dentists.
Likewise, azithromycin and clindamycin have a low incidence of
toxicity and side effects. Clindamycin may cause severe diarrhea,
called pseudomembranous colitis or antibiotic-associated colitis. Several
other drugs such as ampicillin and oral cephalosporins also cause
this problem. However, with clindamycin and other antibiotics, this
problem is usually confined to severely ill and debilitated patients
and is rare in other patients. The elimination of much of the anaerobic gut flora allows the overgrowth of another antibiotic-resistant
bacterium, Clostridium difficile. This bacterium produces toxins that
injure the gut wall, which results in colitis. Patients who take clindamycin, amoxicillin, or cephalosporins should be warned of the possibility of profuse watery diarrhea and should be told to contact their
prescribing dentist if it occurs.
Among the new members of the macrolide (erythromycin) family,
azithromycin has the best combination of effectiveness, low toxicity,
and infrequent drug interactions. Erythromycin is no longer considered effective against the oral pathogens, and it shares with clarithromycin the propensity to cause drug interactions involving the liver
microsomal enzyme system.
Moxifloxacin is a new member of the fluoroquinolone class of
antibiotics that has much better effectiveness against the oral pathogens compared with older members of this class. However, it has
significant toxicities, including muscle weakness and mental clouding, and serious, potentially fatal drug interactions with many commonly used drugs. Moxifloxacin is also contraindicated in children
under 18 years and pregnant females because of interference with the
growth of cartilage. As a new antibiotic, moxifloxacin is expensive.
Moxifloxacin should be reserved for use by specialists treating severe,
recalcitrant infections for which no other effective drug is available.
Oral cephalosporins such as cephalexin and cefadroxil have lost
much of their effectiveness in treating odontogenic infections. These

antibiotics are no longer commonly used for treating odontogenic
infections, even though they are associated with only mild toxicity
problems. As with penicillin, the cephalosporins may cause allergic
reactions. Cephalosporins should be given cautiously to patients with
penicillin allergies because these patients may also be allergic to
cephalosporins. Patients who have experienced an anaphylactic type
of reaction to penicillin should not be given a cephalosporin because
of increased chance for that life-threatening event to recur.
Tetracyclines, like cephalosporins, are no longer considered useful
for treating odontogenic infections, except when they are used topically in very high local concentrations, such as when they are inserted
into periodontal pockets. They have minor toxicities for most patients
(i.e., the commonly encountered GI problems of nausea, abdominal
cramping, and diarrhea). Some patients may experience photosensitivity while they are taking this drug systemically and should be
warned to stay out of the sun. Finally, tetracyclines when taken by
pregnant women may produce tooth discoloration in their infants
when taken by those who are in the tooth development stages of their
lives (under 12 years of age). In the latter case, the discoloration is
the result of chelation of the tetracycline to calcium, which results in
incorporation of the tetracycline into developing teeth.
Metronidazole has mild toxicities, the most prominent being the
typical GI disturbances discussed previously. The drug may also

Chapter | 16 |

produce a disulfiram effect; that is, the patient taking metronidazole
who also consumes ethanol may experience sudden, violent abdominal cramping and vomiting.
Use a bactericidal antibiotic, if possible.  Antibiotics may kill
bacteria (i.e., bactericidal antibiotics) or interfere with their growth
(i.e., bacteriostatic antibiotics). Bactericidal antibiotics usually interfere with cell wall production in newly forming, growing bacteria.
The resultant defective cell wall is not able to withstand the osmotic

pressure differential between the cytoplasm and the environment,
and the bacterial cells lyse (i.e., die). The antibiotic actually kills the
bacteria, so the white blood cells, complement, and antibodies of the
host play a less important role in fighting the bacteria.
Bacteriostatic antibiotics interfere with bacterial reproduction and
growth. This slowing of bacterial reproduction allows host defenses
to move into the area of infection, phagocytize the existing bacteria,
and kill them. Bacteriostatic antibiotics require reasonably intact host
defenses. This type of antibiotic should be avoided in patients who
have compromised host defense systems.
For patients with compromised host defenses, bactericidal antibiotics should be the drugs of choice. For example, the bactericidal
antibiotic penicillin would be preferred over the bacteriostatic
antibiotic azithromycin in a patient who is receiving cancer
chemotherapy.
Be aware of the cost of antibiotics.  Antibiotics vary widely in
cost to patients. Newer-generation drugs tend to be more expensive,
whereas older-generation drugs, which are made by a variety of companies, tend to be less expensive. Generic drugs also tend to be less
expensive than their brand-name counterparts. Generic equivalents
for the newer-generation drugs are not available. When other factors
are equal, the clinician should prescribe the less expensive antibiotic.
Table 16-4 provides a cost comparison among commonly used
antibiotics.
Summary.  Antibiotics should be used to assist the dentist in
treating patients with infections that are spreading beyond the alveolar processes of the jaws and to prevent endocarditis or infection of
prosthetic-implanted devices arising from bacteremia induced by
dental manipulations. Surgical treatment of the infection remains the
primary method of treatment in most patients; antibiotic therapy
plays an adjunctive role. Antibiotics are especially important in
patients who have infections that are spreading beyond the alveolar
process and in patients with compromised host defense mechanisms.

When antibiotic therapy is to be used for treating a routine odontogenic infection, empiric antibiotic therapy with a narrow-spectrum
antibiotic is recommended because the microbiology of odontogenic
infections is well known and usually consistent from patient to
patient. The antibiotic of choice for odontogenic infections is still
a penicillin. The penicillins have been shown to be as effective as
other antibiotics in several prospective studies and systematic reviews.
Penicillins are bactericidal; have a narrow spectrum of action against
pathogens, including streptococci and oral anaerobes, which are
responsible for odontogenic infections; have low toxicity; and are
inexpensive. Among penicillins, amoxicillin may be preferable to
penicillin V because the dosage is less frequent, which increases
compliance with the prescribed regimen, and its cost is often slightly
lower than that of penicillin V.
Although about 25% of Prevotella strains are resistant to penicillins, when used in conjunction with adequate surgery, they almost
always result in cure. Amoxicillin-clavulanate (Augmentin) is a
broad-spectrum penicillin that should be reserved for complex
infections.
Amoxicillin may be used for prophylaxis of endocarditis and late
prosthetic joint infections, according to the formal guidelines of the
ADA in conjunction with the AHA and the American Academy of
Orthopaedic Surgeons (AAOS). An alternative drug is azithromycin,
which is a useful medication for patients who are allergic to

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Part | IV |

Infections

Table 16-4  Cost Comparison of Orally Administered Antibiotics
Antibiotic

Usual Dose

Usual Interval

Weekly Retail Cost, 2011**

Amoxicillin Cost Ratio

Amoxicillin

500 mg

8 hr

$12.19

1.00

Penicillin V

500 mg

6 hr

$12.29

1.01

Augmentin

875 mg

12 hr

$49.79

4.08

2000 mg

12 hr

$99.59

8.17

500 mg

6 hr

$24.29

1.99

Cephalexin Caps (1st)

500 mg

6 hr

$19.89

1.63

Cefadroxil (1st)

500 mg

12 hr

$28.49

2.34

Cefuroxime (2nd)

500 mg

8 hr

$82.99

6.81

Cefaclor ER (generic)

500 mg

12 hr

$64.59

5.30

Cefdinir (3rd)

600 mg

24 hr

$68.99

5.66

Erythromycin base

500 mg

6 hr

$39.19

3.21

Clarithromycin (Biaxin XL)

500 mg

24 hr

$33.59

2.76

Azithromycin (Zithromax)

250 mg

12 hr

$88.99

7.30

Telithromycin (Ketek)

800 mg

24 hr

$93.59

7.68

Clindamycin (generic)

150 mg

6 hr

$28.99

2.38

Clindamycin (2 T generic)

300 mg

6 hr

$54.59

4.48

Clindamycin (generic)

300 mg

6 hr

$74.59

6.12

Metronidazole

500 mg

6 hr

$29.99

2.46

Trimethoprim/Sulfamethoprim

160/800

12 hr

$11.99

0.98

Vancomycin

125 mg

6 hr

$878.99

72.11

Ciprofloxacin

500 mg

12 hr

$24.99

2.05

Moxifloxacin (Avelox)

400 mg

24 hr

$152.99

12.55

Doxycycline

100 mg

12 hr

$11.99

0.98

Linezolid (Zyvox)

600 mg

12 hr

$1,495.99

122.72

Penicillins

Augmentin XR
Dicloxacillin

Cephalosporins (generation)

Erythromycins

Anti-anaerobic

Other

Usual doses and intervals are for moderate infections and are not to be considered prescriptive.
Amoxicillin Cost Ratio = Retail Cost of Antibiotic for 1 week/Retail Cost of Amoxicillin for 1 week.
**Retail Cost/1 week = Retail price charged for a 1-week prescription at a large national pharmacy chain. (Courtesy of Tricia McKinley, CHPT and Rachel Ouellette,
CHPT.)

penicillin. Clindamycin is also a useful alternative for patients with
penicillin allergy or in special situations in which resistant anaerobic
bacteria are suspected. Metronidazole may be useful, especially when
anaerobic bacteria are suspected. It may be used in combination with
another antibiotic that kills facultative and aerobic oral pathogens.

Because of the need to limit the development of resistance and
because of its toxicities and drug interactions, moxifloxacin should
be restricted to prescription by only specialists in the treatment of
severe infections.

310

Principle 7: Administer Antibiotic Properly
Once the decision is made to prescribe an antibiotic to the patient,
the drug should be administered in the proper dose and at the proper
dose interval. The manufacturer usually recommends the proper
dosage and administration. Provision of plasma levels that are sufficiently high to kill the bacteria that are sensitive to the antibiotic
but are not so high as to cause toxicity is adequate. The peak plasma
level of the drug should usually be at least four or five times the


Principles of Management and Prevention of Odontogenic Infections
minimal inhibitory concentration for the bacteria involved in the
infection.
Clearly, some patients stop taking their antibiotics after acute
symptoms have subsided and rarely take their drugs as prescribed
after 4 or 5 days. Therefore, the antibiotic that would have the highest
compliance would be the drug that could be given once a day for not
more than 4 or 5 days. Studies have shown that for odontogenic
infections a 3- or 4-day course of a penicillin, combined with
appropriate surgery, has been as effective as a 7-day course of the
antibiotic.
At the clinical follow-up examination, additional prescription of
antibiotics may be necessary in the case of infections that do not
resolve rapidly. The clinician must make it clear to the patient that

the entire prescription must be taken. If for some reason the patient
is advised to stop taking the antibiotic early, all remaining pills or
capsules should be discarded. Patients should be strongly discouraged from keeping small amounts of unused antibiotics to self-treat
a sore throat next winter. Casual self-administration of antibiotics is
not only useless, but also may be hazardous to the health of the
individual as well as that of the community.

Principle 8: Evaluate Patient Frequently
After surgery and antibiotic therapy, the patient should be carefully
monitored for response to treatment and complications. In most situations, the patient should be asked to return to the dentist 2 to 3 days
after completion of the original therapy. Typically, the patient is seen
to be much improved. If therapy had been successful, swelling and
pain would have decreased dramatically. The dentist should check
the I&D site to determine whether the drain should be removed at
this time. Other parameters such as body temperature, trismus, swelling, and the patient’s subjective feelings of improvement, should also
be evaluated.
If response to treatment is not satisfactory, the patient should be
examined carefully for clues to the reason for failure (Box 16-9). The
most common cause of treatment failure is inadequate surgery. A
tooth may have to be re-evaluated for extraction, or an extension of
the infection into an area not detected during the first treatment may
have to be incised and drained. It may be necessary to admit such a
patient to the hospital for purposes of airway security, further surgery,
and intravenous antibiotic therapy.
A second reason for failure is depressed host defense mechanisms.
A review of the patient’s medical history should be performed, and
more careful, probing questions should be asked. In addition to
immunocompromising diseases, conditions that diminish physiologic reserves, for example, dehydration, malnutrition, and pain,
should also be considered and corrected, if necessary.
A third reason for treatment failure is the presence of a foreign

body. Although this is unlikely in an odontogenic infection, the
dentist may consider taking a careful history and a periapical radiograph of the area to ensure that a radiopaque foreign body is not

Box 16-9  Reasons for Treatment Failure
•
•
•
•

Inadequate surgery
Depressed host defenses
Foreign body
Antibiotic-related problems:
• Patient noncompliance
• Drug not reaching site
• Drug dose too low
• Wrong identification of bacteria
• Wrong antibiotic

Chapter | 16 |

present. Dental implants are increasingly common foreign bodies,
and the ability of bacteria to find shelter from the immune system
in the surface gaps and irregularities of an implant can perpetuate
the infection until the implant is successfully débrided or removed.
Finally, the antibiotic that was given to the patient may be problematic. The dentist first ascertains whether the patient has been
compliant with the dose regimen. The patient must have the prescription filled and must take the antibiotic according to directions. Many
patients fail to follow the instructions of their dentists as carefully as
they should. Sometimes, a patient may not have the prescription
filled because he or she cannot afford it. The dentist should use the

most cost-effective antibiotic available and should directly ask the
patient whether or not a particular prescription is affordable. Another
problem to consider is whether the antibiotic reached the infected
area. The penetration of antibiotics into abscess cavities is poor.
Failure of the antibiotic to reach the area may be related to inadequate surgery or drainage, inadequate blood supply to the local area,
or a dose that is too low to be effective against the bacteria. Another
antibiotic-related problem is incorrect identification of causative bacteria. If a culture was not performed at the initial surgical treatment
or if no surgical treatment was done at the initial therapy, the dentist
should obtain a specimen for C&S testing. Finally, it is possible that
the wrong antibiotic was prescribed for the infection, which may be
because of inaccurate identification of bacteria or the increasing antibiotic resistance of oral bacteria. For example, 25% to 35% of Pre­
votella organisms are resistant to penicillin but rarely cause persistent
infection if penicillin is given and adequate surgery is done. However,
if the patient has a persistent, low-grade infection that does not
resolve despite adequate surgery, prescribing an antianaerobic antibiotic such as clindamycin is appropriate.
The clinician must also examine the patient to look specifically
for toxicity reactions and untoward side effects. Patients may report
complaints such as nausea and abdominal cramping but may fail to
associate watery diarrhea with the drug. Specific questions with
regard to expected toxicities is important to their early recognition.
The dentist should also be aware of the possibility of secondary
infections or superinfections. The most common secondary infection
encountered by dentists is oral or vaginal candidiasis. This is the
result of an overgrowth of Candida organisms because the normal
flora has been altered by the antibiotic therapy. Other secondary
infections may arise as normal host flora is altered, but they are not
seen with significant frequency in the management of odontogenic
infections.
Finally, the dentist should monitor the patient carefully once the
infection has resolved to check for recurrent infection. Recurrence

would be seen in a patient who had incomplete therapy for the infection. A variety of factors may account for this. For example, the
patient may have stopped taking the antibiotic too early. The drain
may have been removed too early, allowing the drainage site to seal
too early and re-establishing the infectious process. If infection does
recur, surgical intervention and reinstitution of antibiotic therapy
should be considered.

PRINCIPLES OF PREVENTION OF INFECTION
The use of antibiotics to treat an established infection is a wellaccepted and well-defined technique. These drugs provide major
assistance for the patient in overcoming an established infection. The
use of antibiotics for prevention (i.e., prophylaxis) of infection is less
widely accepted. The final section of this chapter discusses the use of
antibiotics for prophylaxis of two distinct types of infection. The use
of antibiotics to prevent wound infection after surgery is presented
first, followed by a discussion of antibiotic use to prevent metastatic
infection.

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Part | IV |

Infections

PRINCIPLES OF PROPHYLAXIS OF
WOUND INFECTION
On the one hand, the use of antibiotics for prophylaxis of postoperative wound infections may be effective and desirable in certain
situations. On the other hand, little scientific evidence supports
the effectiveness of prophylactic antibiotics in dentistry and oralmaxillofacial surgery. If, however, prophylactic antibiotics are effective in preventing postoperative wound infections and bloodborne
infections of distant sites, they would have three distinct advantages:

(1) Prophylactic antibiotics may reduce the incidence of postoperative infection and, thereby, reduce postoperative morbidity. When a
patient becomes infected after surgery, wound healing and recovery
are substantially delayed. (2) Appropriate and effective antibiotic
prophylaxis may reduce the cost of health care. By decreasing the
incidence of postoperative infection, the patient can be saved the
expense of returning to the dentist, buying more antibiotics, and
missing additional days of work. Third, appropriate use of prophylactic antibiotics requires a shorter-term administration, rather than
therapeutic use, thus possibly decreasing the total amount of antibiotics used by the population.
On the other hand, when they are used inappropriately, prophylactic antibiotics are, actually in fact, associated with an increased risk
of postoperative infection, typically by a bacterium resistant to these
prophylactic antibiotics. The use of prophylactic antibiotics has
several other disadvantages, as discussed earlier. First, they may alter
host flora. The body is populated with a variety of bacteria that have
a symbiotic relationship with the host. When antibiotics are administered, some of these bacteria are eliminated, allowing the overgrowth of antibiotic-resistant and perhaps more pathogenic bacteria
that may then cause infection. Second, as several studies have shown,
antibiotic administration in one patient allows antibiotic-resistant
organisms to spread to the patient’s family and to the community.
Third, in certain situations, the risk of infection is so low that the
antibiotic does not significantly decrease the incidence of infection.
Fourth, the use of prophylactic antibiotics may encourage lax surgical
and aseptic techniques on the part of the dentist. The attitude of, “Oh
well, the patient is on antibiotics,” is an unacceptable excuse when
the principles of atraumatic tissue handling and surgical asepsis are
violated. Fifth, the cost of the antibiotic must be considered. Although
the cost for a single event for a single patient may be small, the cost
for many surgeries for many patients can be enormous. Finally, the
toxicity of the drug to the patient must be also kept in mind. All drugs
have the potential to cause injury to the patient. Although most
antibiotics used by dentists have low toxicity, the possibility of toxicity is always present. The principles of prophylactic antibiotic use are
summarized in Box 16-10.

Principle 1: Procedure Should Have
Significant Risk of Infection
To justify the prophylactic administration of antibiotics to reduce the
incidence of infection, the surgical procedure must have a high

Box 16-10  Principles of Prophylactic Antibiotic Use
•
•
•
•
•

312

Find out if the risk of infection is significant.
Choose the correct narrow-spectrum antibiotic.
Confirm that the antibiotic level is high.
Ensure that the antibiotic is in the target tissue before surgery.
Use the shortest effective antibiotic exposure.

enough incidence of infection. Clean surgery done with strict adherence to basic surgical principles usually has an incidence of infection
of about 3%. Infection rates of 10% or more are usually considered
unacceptable, and the prophylactic use of antibiotics must be strongly
considered for such infection-prone procedures. For the dentist doing
routine office surgery, this means that most office procedures performed on healthy patients do not require prophylactically administered antibiotics. The incidence of infection after tooth extraction,
frenectomy, biopsy, minor alveoloplasty, and torus reduction is
extremely low; therefore, antibiotics would provide no benefit. This
is true even in the presence of periapical infection, severe periodontitis, and multiple extractions.
However, several surgical factors may influence the dentist to

strongly consider the use of antibiotic prophylaxis (Box 16-11): The
first and most obvious factor that may lead to infection is a bacterial
inoculum of sufficient size. The usual surgical procedure performed
in the mouth rarely involves sufficient bacterial inoculation to cause
infection unless an acute infection with cellulitis or an abscess is
already present. The second factor is surgery that involves a prolonged procedure. In hospital surgeries, the incidence of postoperative infection increases significantly with operations lasting longer
than 4 hours. A third factor that may prompt the use of antibiotics
is the insertion or presence of a foreign body, most commonly a
dental implant. Most data seem to suggest that the use of antibiotics
may decrease the incidence of infection when foreign bodies such as
dental implants are inserted into the jaws.
The final and most important factor for most dentists in determining which patients should receive prophylactic antibiotics is whether
the patient’s host defenses are depressed. Patients who have a compromised ability to defend themselves against infection should
receive antibiotics prophylactically because they are likely to have a
higher incidence of more severe infection. All patients receiving
cancer chemotherapy or immunosuppressives should receive anti­
biotics prophylactically, even when minor surgical procedures are
performed. Patients receiving immunosuppressives for organ transplantation will be taking these drugs for the remainder of their lives
and should be given preventive antibiotics accordingly. Patients
receiving cancer chemotherapy will receive cytotoxic drugs for 1 year
or less, but should be given antibiotics prophylactically for at least a
1-year period after the cessation of their chemotherapy. This is also
advisable for those receiving radiation therapy to the jaw. Patients
with end-stage renal disease, including those receiving kidney dialysis, are immunocompromised and require antibiotic prophylaxis for
oral surgical procedures.
The most common immunocompromising disease, however, is
diabetes mellitus. The incidence of postoperative infection in persons
with diabetes is directly correlated with elevations of blood sugar.
The oral surgical management of persons with diabetes based on
their blood glucose is summarized in Table 16-5. The glycosylated

hemoglobin test, or hemoglobin A1c, is a good measure of the level
of diabetes control over the previous 3 to 4 months. Before complex
reconstructive oral-maxillofacial surgery such as the placement of
dental implants, the dentist is wise to ensure that acceptable
intermediate-term control of blood glucose has been achieved, as
measured by a hemoglobin A1c of 7% or less. The American Diabetes
Association recommends a therapeutic target hemoglobin A1c level

Box 16-11  Factors Related to Postoperative Infection
•
•
•
•

Size of bacterial inoculum
Duration of surgery
Presence of foreign body, implant, or dead space
State of host resistance


Principles of Management and Prevention of Odontogenic Infections

Table 16-5  Dental Treatment for Patients with Diabetes,
Based on Fingerstick Blood Glucose Testing
Finger Stick Blood
Glucose (mg/dL%)

Dental Treatment

Less than 85

Administer glucose; postpone elective
treatment

85–200

Stress reduction; consider antibiotic
prophylaxis for extraction

200–300

Stress reduction; antibiotic prophylaxis;
referral to primary care physician

300–400

Avoid elective treatment; referral to
primary care physician or emergency
room at nearby hospital

Greater than 400

Avoid elective treatment; send to
emergency room at nearby hospital

of 7% or less. Withholding dental implant therapy and working with
the patient’s physician can help motivate the patient to achieve effective long-term control of diabetes. Although prophylactically administered antibiotics are helpful in patients with diabetes, perioperative
control of blood sugar levels is paramount.

Principle 2: Choose Correct Antibiotic

The choice of antibiotic for prophylaxis against infections after
surgery of the oral cavity should be based on the following criteria:
First, the antibiotic should be effective against the organisms most
likely to cause infection in the oral cavity. As previously discussed,
facultative streptococci are usually the originally invading organism
in oral infection. Second, the antibiotic chosen should be a narrowspectrum antibiotic.
By using a narrow-spectrum antibiotic, the risk of altering host
flora is minimized. Third, the antibiotic should be the least toxic
antibiotic available for the patient. Finally, the drug selected should
be a bactericidal antibiotic. Because many of the routine prophylactic
uses of antibiotics in the dental office are for patients with compromised host defenses, it is important to ensure that the antibiotic
effectively kills the bacteria.
Taking into account these four criteria, the antibiotic of choice for
prophylaxis before oral surgery is penicillin or amoxicillin. These two
antibiotics are effective against the causative organism (i.e., Streptococ­
cus), have a narrow spectrum of activity, have low toxicity, and are
bactericidal. For patients allergic to penicillin, the best choice is
clindamycin. Clindamycin is a narrow-spectrum antibiotic, fairly
effective against oral streptococci, and is bacteriostatic. The third
choice for oral administration for prophylaxis is azithromycin.
Azithromycin, another narrow-spectrum antibiotic, is reasonably
effective against the usual organisms, and it is also bacteriostatic.

Principle 3: Antibiotic Plasma Level Must
Be High
When antibiotics are used prophylactically, the antibiotic level in the
plasma must be higher than when antibiotics are used therapeutically. The peak plasma levels should be high to ensure diffusion of
the antibiotic into all of the fluid and tissue spaces where the surgery
is going to be performed. The usual recommendation for prophylaxis

Chapter | 16 |

is that the drug be given in a dose at least two times the usual therapeutic dose. Use of the same prophylactic doses recommended by
the AHA for prophylaxis of infective endocarditis is reasonable. For
penicillin or amoxicillin, this is 2 g; for clindamycin, 600 mg; and
for azithromycin, 500 mg.

Principle 4: Time Antibiotic Administration
Correctly
For the antibiotic to be maximally effective in preventing postoperative infection, the antibiotic must be given 2 hours or less before the
surgery begins. The time of dosing before surgery varies, depending
on the route used, allowing for absorption of the antibiotic into
tissues at the time of wounding. For the oral route, this is usually 1
hour; with the intravenous route, a much shorter preoperative dosing
interval is possible. This principle has been clearly established in
many animal and human clinical trials. Antibiotic administration
that occurs after surgery is greatly decreased in its efficacy or has no
effect at all on preventing infection; evidence indicates that prophylactically administered antibiotics given 2 hours or more after surgery
may increase the risk of wound infection.
If the surgery is prolonged and an additional antibiotic dose is
required, intraoperative dose intervals should be shorter (i.e., one
half the usual therapeutic dose interval). Therefore, penicillin and
clindamycin should be given every 3 hours during prolonged surgery.
This ensures that the peak plasma levels will stay adequately high
and avoids periods of inadequate antibiotic levels in the tissue fluids.

Principle 5: Use Shortest Antibiotic
Exposure That Is Effective
For the antibiotic prophylaxis to be effective, the antibiotic must be
given before the surgery begins, and adequate plasma levels must be

maintained during the surgical procedure. Once the surgical procedure is completed, continued antibiotic administration produces
little, if any, benefit. If the procedure is a short operation, a single
preoperative dose of antibiotics is adequate. Considerable amounts
of animal and human clinical data demonstrate that the prophylactic
use of antibiotics is necessary only for the time of surgery; after
closure of the wounds and formation of the blood clots, migration
of bacteria into the wound and underlying tissues occurs at such a
low level that additional antibiotics are not necessary.

Summary
The use of antibiotics for prophylaxis of postoperative wound infection may be effective. It may reduce patient pain, morbidity, cost, and
total antibiotic use. Appropriate antibiotic prophylaxis does little to
alter host flora. Most dental procedures on healthy patients do not
require antibiotic prophylaxis. A few select patients who are to
undergo long surgical procedures or the insertion of foreign bodies
such as dental implants should be considered for prophylaxis.
Patients who have compromised host defenses because of poorly
controlled metabolic diseases or certain diseases that interfere with
host defenses or who are taking drugs that suppress the immune
system should also be given prophylactic antibiotics. The drug of
choice is a narrow-spectrum antibiotic that is effective against causative organisms, is nontoxic, and is bactericidal. Penicillin fits these
criteria the best.
When the antibiotic is given, it should be taken before the surgery
begins, at a normal dose twice that of therapeutically administered
antibiotics. If the surgery is prolonged, interim doses at half the
normal dose interval should be used. High plasma levels should be

313

Part | IV |

Infections

maintained during the surgical procedure, but no additional antibiotics are necessary after surgery.

PRINCIPLES OF PROPHYLAXIS AGAINST
METASTATIC INFECTION
Metastatic infection is defined as infection that occurs at a location
physically separate from the portal of entry of the bacteria. The classic
and most widely understood example of this phenomenon is bacterial endocarditis, which may arise from bacteria that are introduced
into the circulation as a result of tooth extraction, for example. The
incidence of metastatic infection can be reduced if antibiotic administration is used to eliminate the bacteria before they can establish
an infection at the remote site.
For metastatic infection to occur, several conditions must be met
(Box 16-12). The first and most important is a susceptible location
in which an infection can be established. An example of this is the
deformed heart valve with its altered endothelial surface onto which
an irregularly surfaced vegetation has formed.
Bacterial seeding of the susceptible area must also take place. This
seeding occurs as the result of a bacteremia in which bacteria from
the mouth are carried to the susceptible site. Most likely, a quantitative factor is involved in this seeding process because the body experiences multiple episodes of small bacteremias as a result of normal
daily activities such as chewing and toothbrushing. Turbulent blood
flow across a deformed heart valve can traumatize the endothelial
lining of the valve, which can then precipitate the deposition of
platelets and fibrin, resulting in nonbacterial thrombotic endocarditis (NBTE). Subsequently, bacterial proteins, called adhesins, recognize the fibrin and platelet matrix of NBTE. Some staphylococci and
oral streptococci, especially Streptococcus sanguis, Streptococcus mitis,
and Streptococcus oralis, have these adhesins, which explains their
association with infective endocarditis.
Also necessary for the establishment of metastatic infection is

some impairment of the local host defenses. Once bacteria have
attached to NBTE, they are protected from white blood cell phagocytosis by a thin coating of fibrin and an extracellular matrix synthesized by bacteria, resulting in a biofilm. More than 90% of the
bacteria existing within a mature cardiac vegetation are in a metabolically inactive state, which also renders them less susceptible to bactericidal antibiotics. Bacteria inhabiting such a biofilm coating on
foreign bodies such as a prosthetic joint or dental implants are not
easily phagocytized by white blood cells or killed by antibiotics, as
in endocarditis.

Prophylaxis Against Infectious Endocarditis
Historically, the rationale for antibiotic prophylaxis of infectious
endocarditis (IE) after dental procedures has been based on the following facts: Bacteremias have been shown to cause IE; viridansgroup streptococci are part of the normal oral flora and have been
commonly found in IE; dental procedures can cause bacteremias
because of Streptococcus viridans; a large number of case reports associate dental procedures with subsequent IE; S. viridans is generally

Box 16-12  Factors Necessary for Metastatic Infection
• Distant susceptible site
• Hematogenous bacterial seeding
• Impaired local defenses

314

susceptible to the antibiotics recommended for prophylaxis of IE;
antibiotic prophylaxis has been shown to prevent experimental endocarditis caused by S. viridans in animals; the risk of significant adverse
reaction to the antibiotic is low in an individual patient, and the
morbidity and mortality of IE are high. When this occurs, the patient
must be treated in the hospital with high doses of intravenous antibiotics for prolonged periods. Often, the damaged native heart valve
must be surgically replaced with a prosthetic valve. Although initial
recovery from bacterial endocarditis approaches 100%, recurrent episodes reduce the 5-year survival rate of patients with this disease to
approximately 60%.
Recent evidence puts into question the likelihood, however, that
prophylactic antibiotics prevent IE in human beings. Antibiotics do

not consistently prevent bacteremias after dental procedures. Bacteremias after chewing, toothbrushing, and other daily activities occur
far more frequently than after dental procedures. Endocarditis has
been shown to occur despite appropriate antibiotic prophylaxis for
dental procedures. Only a small proportion of IE cases are from
dental procedures, and very few cases of IE would be prevented by
antibiotic prophylaxis for dental procedures, even it if were 100%
effective.
The AHA has had formal recommendations for the prevention of
IE after dental treatments since 1960. The latest formal recommendations appeared in May 2007. Dentists must stay abreast of revised
recommendations as they are published by the AHA and the ADA.
These new guidelines take into account that a very small number of
cases of IE might be caused by dental procedures and might be prevented by antibiotic prophylaxis. New emphasis has been correctly
placed on the establishment and maintenance of optimal oral health
in patients with increased risk for IE.
The new guidelines indicate prophylaxis only for the patients at
highest risk of endocarditis, including those with previous endocarditis, prosthetic heart valves, cyanotic congenital heart defects that
have not been repaired or have remaining partial defects after repair,
and heart transplant patients with valvulopathy. This will significantly decrease the number of dental patients for whom prophylaxis
is indicated. A list of the conditions that pose the highest risk of
endocarditis can be found in Box 16-13.
Recent evidence also indicates that the magnitude of bacteremia
caused by a given dental procedure is not necessarily correlated with

Box 16-13  Cardiac Conditions Associated with the
Highest Risk of Adverse Outcome from
Endocarditis for Which Prophylaxis with
Dental Procedures Is Recommended
• Prosthetic cardiac valve
• Previous infective endocarditis
• Congenital heart disease (CHD)*

• Unrepaired cyanotic CHD, including palliative shunts and
conduits
• Completely repaired congenital heart defect with prosthetic
material or device, whether placed by surgery or by catheter
intervention, during the first 6 months after the procedure†
• Repaired CHD with residual defects at the site or adjacent to
the site of a prosthetic patch or prosthetic device (which
inhibit endothelialization)
• Cardiac transplant recipients who have cardiac valvulopathy
*Except for the conditions listed above, antibiotic prophylaxis is no longer
recommended for any other form of CHD.
†
Prophylaxis is recommended because endothelialization of prosthetic material
occurs within 6 months after the procedure.


Principles of Management and Prevention of Odontogenic Infections

Box 16-14  Dental Procedures for Which Endocarditis
Prophylaxis Is Recommended for Patients
in Box 16-13

Table 16-6  Antibiotic Regimens for Prophylaxis of
Bacterial Endocarditis
REGIMEN
30–60 MIN BEFORE
PROCEDURE

All dental procedures that involve manipulation of gingival tissue or
the periapical region of teeth or perforation of the oral mucosa.*

*The following procedures and events do not need prophylaxis: routine
anesthetic injections through noninfected tissues, taking dental radiographs,
placement of removable prosthodontic or orthodontic appliances, adjustment
of orthodontic appliances, placement of orthodontic brackets, shedding of
deciduous teeth, and bleeding from trauma to the lips or oral mucosa.

Box 16-15  Dental Procedures in Which Prophylaxis Is
Not Recommended
•
•
•
•
•
•
•
•
•
•

Restorative dentistry
Routine local anesthetic injection
Intracanal endodontic therapy and placement of rubber dams
Suture removal
Placement of removable appliances
Making of impressions
Taking of oral radiographs
Fluoride treatments
Orthodontic appliance adjustment
Shedding of primary teeth

the incidence of IE. Therefore, the new guidelines have simplified the
description of dental procedures for which antibiotic prophylaxis
should be used to the following description: “All dental procedures
that involve manipulation of gingival tissue or the periapical region
of teeth or perforation of the oral mucosa” (Box 16-14). Prophylaxis
is not required for routine local anesthetic injections through
noninfected tissue, dental radiographs, placement of removable
prosthodontic or orthodontic appliances, adjustment of orthodontic
appliances, placement of orthodontic brackets, shedding of decid­
uous teeth, and bleeding from trauma to the lips or oral mucosa
(Box 16-15).
Bacterial endocarditis prophylaxis is achieved for most routine
conditions with the administration of 2 g of amoxicillin orally a half
hour to 1 hour before the procedure (Table 16-6). Amoxicillin is the
drug of choice because it is better absorbed from the GI tract and
provides higher and more sustained plasma levels. Amoxicillin is an
effective killer of viridans-group streptococci, which include the
organisms that most commonly cause IE after bacteremias from the
oral cavity.
For patients who are allergic to penicillin, two alternative drugs
have been recommended. The first recommended drug is clindamycin, with a dose of 600 mg orally 1 hour before surgery. If the patient’s
allergy to penicillin is mild and not of an anaphylactic type, a firstgeneration cephalosporin such as cephalexin may be prescribed.
Although erythromycin is no longer recommended, the newer macrolide antibiotics, azithromycin or clarithromycin, are acceptable
alternative drugs. If the patient is unable to take oral medication,
parenteral administration can be used.
For the pediatric patient, the dose of the drugs that are given must
be reduced. The recommendations include clear guidelines for proper
pediatric dosing (see Table 16-6).

Chapter | 16 |

Situation

Agent

Adults

Children*

Oral

Amoxicillin

2 g

50 mg/kg

Parenteral

Ampicillin

2 g IM or IV

Cefazolin/
ceftriaxone†

1 g IM or IV

50 mg/kg
IM or IV

50 mg/kg
IM or IV

Cephalexin†

2 g

50 mg/kg

Clindamycin
Azithromycin/
clarithromycin

600 mg
500 mg

20 mg/kg
15 mg/kg

Cefazolin/
ceftriaxone†

1 g IM or IV

50 mg/kg
IM or IV

Clindamycin

600 mg IM

or IV

20 mg/kg
IM or IV

Penicillin
allergy,
oral

Penicillin
allergy,
parenteral

*Total children’s dose should not exceed adult dose.
†
Cephalosporins should not be used in patients with immediate-type
hypersensitivity reaction to penicillins. Other first-generation or secondgeneration oral cephalosporins may be substituted in equivalent adult or
pediatric doses.
IM, Intramuscularly; IV, intravenously.

Some patients at risk for bacterial endocarditis may be taking daily
doses of penicillin to prevent recurrence of rheumatic fever or may
already be taking an antibiotic for other reasons. In these patients,
the streptococci may be relatively resistant to penicillin. The recommendation for this situation is that the dentist should use clindamycin, azithromycin, or clarithromycin for prophylaxis of endocarditis.
The cephalosporins should be avoided because of possible crossresistance with the penicillins. If possible, the procedure should be
postponed until 10 or more days after the antibiotic is completed,
thus allowing a more normal oral flora to be re-established.
If a particular patient requires a series of dental treatments that
requires antibiotic prophylaxis, a period of 10 or more days between
appointments is appropriate. The reason for the interval is that the

continuous administration of antibiotics for several days or more
may promote colonization of the patient by bacteria that are resistant
to the antibiotic being given, thus making prophylaxis more likely to
fail. The 10-or-more day antibiotic-free period may allow antibioticsensitive organisms to repopulate the oral flora. However, it has been
shown that baseline antibiotic resistance levels are not re-established
for several months after a course of antibiotics. For this reason, the
number of dental visits should also be minimized, consistent with
the patient’s tolerance level.
Occasionally, unexpected bleeding may occur during dental treatment in a patient who is at risk for endocarditis, or a patient may not
inform the dentist of the indication for antibiotic prophylaxis before
the beginning of the procedure. In this situation, appropriate antibiotic prophylaxis should be administered as soon as possible. Prophylaxis given longer than 4 hours after the bacteremia may have limited
prophylactic benefit.
Patients at risk for IE should have a comprehensive prophylaxis
program that includes excellent oral hygiene with excellent periodic

315


Part | IV |

Infections

professional care. Special care should be taken for the establishment
of an effective preventive program, and all incipient dental and periodontal disease should be treated. If surgery is required, the mouth
can be rinsed preoperatively with an antibacterial agent such as
chlorhexidine. Preoperative oral antiseptic rinses have been shown to
reduce the magnitude of bacteremias (the number of bacteria entering the bloodstream), although they are not a substitute for antibiotic
prophylaxis.
Finally, it is important for the dentist to understand that even
when appropriate measures are taken to prevent bacterial endocarditis, it may still occur. Patients should be informed of this and advised

to return to the dentist or to their primary care physician if any of
the signs and symptoms of bacterial endocarditis, especially fever and
malaise, occur.
Prosthetic valve endocarditis occurs when the tissue around the
cardiac valve implant becomes infected. Such infections are caused
by the same bacteria that cause typical native valve endocarditis.
Prosthetic valve endocarditis is a much more serious illness than
native valve endocarditis because loosening of the heart valve may
result in death. The 1-year survival rate for patients who have prosthetic valve endocarditis is about 50%. The AHA currently states that
the standard oral regimens are adequate for most patients with prosthetic heart valves.

Prophylaxis in Patients with Other
Cardiovascular Conditions
Several other cardiovascular conditions require the clinician to consider the administration of prophylactic antibiotics for the prevention of metastatic infection. In coronary artery bypass grafting
(CABG), the coronary arteries are reconstructed with vascular grafts.
Because CABG does not predispose patients to metastatic infection,
these patients should not be given prophylactic antibiotics before a
dental procedure is performed.
Patients with a transvenous pacemaker have a battery pack
implanted in their chests, with a thin wire that runs through the
superior vena cava into the right side of the heart. These patients do
not require prophylactic antibiotics when dental procedures are performed. Similarly, coronary artery angioplasty, with or without stent
placement, is not an indication for endocarditis prophylaxis.
Patients receiving renal dialysis frequently have an arteriovenous
shunt surgically constructed in their forearms to provide the dialysis
team ready access to the bloodstream. Metastatic infection may occur
in these shunts after bacteremia. Therefore, the dentist should contact
the patient’s nephrologist or renal dialysis team to discuss the best
management.
Patients who have hydrocephaly may have decompression with

ventriculoatrial shunts. Because these shunts may induce valvular
dysfunction, antibiotic prophylaxis may be required. Consultation
with the patient’s neurosurgeon should be considered.
Patients who have had severe atherosclerotic vascular disease and
have had alloplastic vascular grafts placed to replace portions of their
arteries do not appear to be at risk for metastatic infection from
dental procedures. Therefore, the AHA does not recommend antibiotic prophylaxis for nonvalvular cardiovascular devices, including
coronary artery stents and vena caval filters. The exception to this rule
is for I&D of abscesses at other sites, including the oral cavity.

Prophylaxis Against Total Joint
Replacement Infection
Patients who have undergone total replacement of a joint with a
prosthetic joint may be at risk for hematogenous spread of bacteria

316

and subsequent infection. These late prosthetic joint infections result
in severe morbidity because the implant is usually lost when infections occur. There has been great concern that the bacteremia caused
by tooth extraction may result in such infections. However, the recent
literature suggests that bacteremias from oral procedures are not
likely to cause prosthetic joint infections. It appears that the bacteremia after oral surgery is of a transient nature and does not expose the
implant and periimplant tissues to bacteria long enough to cause
infection.
Instead it appears that the hematogenous spread of prosthetic
joint infections is caused by chronic infections elsewhere in the
body that result in chronic septicemias. These infections are typically
urogenital, gastrointestinal, pulmonary, or skin infections, but
established odontogenic infections may also cause a septicemia
of sufficient magnitude to cause a total joint infection.

In 2003 the American Dental Association (ADA) and the Amer­
ican Academy of Orthopaedic Surgeons (AAOS) issued a revised
joint recommendation concerning the management of patients with
prosthetic total joints. In 2009, the American Academy of Ortho­
paedic Surgeons issued an advisory statement recommending that
all patients with prosthetic joints receive antibiotic prophylaxis
before dental procedures, regardless of the length of time following
implantation.
This apparent controversy has been resolved by the joint publication of an evidence-based guideline and report that evaluates the
currently available scientific evidence on the causation of late prosthetic joint infections following dental procedures. The 3 recommendations of the American Dental Association and the American
Academy of Orthopaedic Surgeons are:
1. The practitioner might consider discontinuing the practice
of routinely prescribing prophylactic antibiotics for
patients with hip and knee prosthetic joint implants
undergoing dental procedures. (Strength of
Recommendation: Limited)
2. We are unable to recommend for or against the use of topical
oral antimicrobials in patients with prosthetic joint implants or
other orthopaedic implants undergoing dental procedures.
(Strength of Recommendation: Inconclusive)
3. In the absence of reliable evidence linking poor oral health to
prosthetic joint infection, it is the opinion of the work group
that patients with prosthetic joint implants or other orthopaedic
implants maintain appropriate oral hygiene. (Strength of
Recommendation: Consensus)
The report also states: “Practitioners should be cautious in deciding whether to follow a recommendation classified as Limited, and
should exercise judgment and be alert to emerging publications that
report evidence. Patient preference should have a substantial influencing role.”
The first recommendation is classified as limited because the
limited amount of currently available reliable scientific evidence does

not substantiate that dental procedures cause late prosthetic joint
infections. It further does not indicate that antibiotic prophylaxis
reliably prevents such infections. The limited available data is inconclusive, but points toward a lack of causation of late prosthetic joint
infection by dental procedures. Therefore the use of prophylactic
antibiotics before dental procedures is not justified by the scientific
evidence available to date.
The second recommendation is classified as inconclusive because
the studies performed to date have come to inconsistent conclusions,
from which no clear recommendation can be generated.
The third recommendation is based upon the consensus of the
expert panel, rather than on any scientific studies.
Recently published case series have not found any association
between late prosthetic joint infection and dental procedures,
whether antibiotic prophylaxis was used or not. These studies must


Principles of Management and Prevention of Odontogenic Infections
be interpreted with caution, however, because they did not distinguish between prosthetic joint infections caused by oral pathogens
and those caused by other pathogens, such as Staphylococcus aureus,
the source of which primarily is the skin.
When considering the use of a prophylactic antibiotic in the
patient with a prosthetic joint, the clinician must weigh the risk of
allergic reaction to the antibiotic, the development of antibiotic resistance in the host and in the community, and the cost against the low
incidence of prosthetic joint infections, the questionable causation of
these infections by dental procedures, and the lack of proven effectiveness of antibiotic prophylaxis in preventing these infections.
Until determinative scientific evidence is available, the clinician
must use sound judgment in deciding whether to use antibiotic
prophylaxis in the patient with a prosthetic joint.
When there is disagreement between the dentist, the patient, or
the patient’s physician over the need for antibiotic prophylaxis, clear

Chapter | 16 |

communication between all parties is required to clarify all relevant
facts, the recommendations of professional associations, and scientific data and to arrive at a consensus. Ultimately, the dentist is
responsible for his or her own treatment decisions and should not
render care that he or she thinks is not in the best interest of the
patient.
If a patient who has a total joint replacement needs treatment of
an established odontogenic infection, aggressive therapy for the
infection is necessary to prevent seeding of the bacteria into the
prosthesis, causing odontogenic infection of the prosthetic joint. This
aggressive treatment should include extraction, I&D, and the use of
high-dose bactericidal antibiotics, possibly given IV. The clinician
should strongly consider performing C&S testing because if a prosthetic joint infection does occur, it would be useful to know which
bacteria are likely the causative organisms along with their antibiotic
sensitivity.

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Part | IV |

Infections

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Chapter

17 

Complex Odontogenic Infections
Thomas R. Flynn

CHAPTER OUTLINE
DEEP FASCIAL SPACE INFECTIONS  319
Infections Arising from any Tooth  320
Infections Arising from Maxillary Teeth  320
Infections Arising from Mandibular Teeth  325
Deep Cervical Fascial Space Infections  330
Management of Fascial Space Infections  331
OSTEOMYELITIS  333
ACTINOMYCOSIS  335
CANDIDIASIS  336
Odontogenic infections are usually mild and readily treated with the
appropriate surgical procedure with or without supplemental antibiotic therapy. Infections that spread beyond teeth into the oral vestibule are usually managed by intraoral incision and drainage (I&D)

procedures, as well as dental extraction, root canal therapy, or gin­
gival curettage, as appropriate. The principles of management of
routine odontogenic infections are discussed in Chapter 16. Some
odontogenic infections are serious and require management by oralmaxillofacial surgeons, who have extensive training and experience
in this area. Even after the advent of antibiotics and improved dental
health, serious odontogenic infections still sometimes result in death.
These deaths occur when the infection reaches areas distant from the
alveolar process. The purpose of this chapter is to present an overview
of deep fascial space infections of the head and neck originating in
teeth, as well as several less common but important infections of the
oral cavity.

DEEP FASCIAL SPACE INFECTIONS
The pathways of odontogenic infection extending from the teeth
through bone and into surrounding soft tissues are discussed in
Chapter 16. As a general rule, infection erodes through the thinnest
adjacent bone and causes infection in the adjacent tissue. Whether

this becomes a vestibular or a deeper fascial space abscess is determined primarily by the relationship of the attachment of the nearby
muscles to the point at which the infection perforates the bony cortical plate. Most odontogenic infections penetrate the facial cortical
plate of bone to become vestibular abscesses. On occasion, infections
erode into other deep fascial spaces directly (Fig. 17-1). Fascial spaces
are fascia-lined tissue compartments filled with loose, areolar connective tissue that can become inflamed when invaded by microorganisms. The resulting process of inflammation passes through stages
that are seen clinically as edema (inoculation), cellulitis, and abscess.
In healthy persons, the deep fascial spaces are only potential spaces
that do not exist. The loose areolar tissue within these spaces serves
to cushion the muscles, vessels, nerves, glands, and other structures
that it surrounds and to allow relative movement between these
structures. During an infection, this cushioning and lubricating tissue
has the potential to become greatly edematous in response to the

exudation of tissue fluid and then to become indurated when polymorphonuclear leukocytes, lymphocytes, and macrophages migrate
from the vascular space into the infected interstitial spaces. Ultimately, liquefactive necrosis of white blood cells and this connective
tissue leads to abscess formation, and spontaneous or surgical drainage typically leads to resolution. This is the pathophysiology of the
stages of infection that clinicians see as edema, when bacteria inoculate the tissues of a particular anatomic space; cellulitis, when an
intense inflammatory response causes all of the classic signs of
inflammation and abscess, when small areas of liquefactive necrosis
coalesce centrally to form pus within tissues.
On the basis of the relationship between the point at which the
infection erodes through alveolar bone and surrounding muscle
attachments, infections arising from any maxillary or mandibular
tooth can cause vestibular, buccal, or subcutaneous space infections.
Infections passing beyond the alveolar process on the deep (toward
the oral cavity) side of the nearby muscle of facial expression invade
the vestibular space, and those that enter soft tissue on the superficial
(toward skin) side of those muscles enter the buccal or the subcutaneous space. Infections arising from maxillary teeth also tend to spread
into the infraorbital, palatal, orbital, and infratemporal spaces, and
the maxillary sinus (Box 17-1). Mandibular dental infections also
tend to spread into the submandibular, sublingual, submental, and

319